Đang tải... (xem toàn văn)
(BQ) Part 2 book ASE''s Comprehensive echocardiography textbook presents the following contents: Aortic stenosis, aortic regurgitation, mitral stenosis, pulmonic regurgitation, prosthetic valves, mitral regurgitation, infective endocarditis, pericardial diseases,...
Section Aortic Stenosis XV 94 Aortic Stenosis Morphology Steven A Goldstein, MD CONGENITAL AORTIC STENOSIS Natural History of Bicuspid Aortic Valves Bicuspid Aortic Valve Although a few patients with BAV may go undetected or without clinical consequences for a lifetime, most will develop complications The most important clinical consequences of BAV are valve stenosis, valve regurgitation, infective endocarditis, and aortic complications such as dilatation, dissection, and rupture (Box 94.2) Estimates of the prevalence of these complications and outcomes have varied depending on the era of the study, the cohort selected, and the method used to diagnose BAV (clinical exam vs cardiac catheterization vs echocardiography) Several large recent studies have helped to better define the unoperated clinical course in the modern era.17–19 Isolated AS is the most frequent complication of BAV, occurring in approximately 85% of all BAV cases.10,18–20 Bicuspid aortic valve accounts for the majority of patients aged 15 to 65 years with significant AS The progression of the congenitally deformed valve to AS presumably reflects its propensity for premature fibrosis, stiffening, and calcium deposition in these structurally abnormal valves Aortic regurgitation, present in approximately 15% of patients with BAV,10 is usually due to dilation of the sinotubular junction of the aortic root, preventing cusp coaptation It may also be caused by cusp prolapse, fibrotic retraction of the leaflet(s), or damage to the valve from infective endocarditis Aortic regurgitation tends to occur in younger patients than does AS Why some patients with a BAV develop stenosis and others regurgitation is not clear As mentioned, rarely, patients may not develop hemodynamics consequences Roberts and colleagues reported three congenital BAVs in nonagenarians who underwent surgery for AS.21 Why some patients with a congenital BAV not become symptomatic until they are in their 90s and why others become symptomatic in early life is also unclear Congenital aortic valve malformation reflects a phenotypic continuum of unicuspid valve (severe form), bicuspid valve (moderate form), tricuspid valve (normal, but may be abnormal), and the rare quadricuspid forms Bicuspid aortic valves (BAVs) are the result of abnormal cusp formation during the complex developmental process In most cases, adjacent cusps fail to separate, resulting in one larger conjoined cusp and a smaller one Therefore, BAV (or bicommissural aortic valve) has partial or complete fusion of two of the aortic valve leaflets, with or without a central raphe, resulting in partial or complete absence of a functional commissure between the fused leaflets.1 The generally accepted prevalence of BAV in the general population is 1% to 2%, making it the most common congenital heart defect Information on the prevalence of BAV comes primarily from pathology centers.1–7 Valvular aortic stenosis (AS), a chronic progressive disease, usually develops over decades Box 94.1 lists the most common etiologies of valvular AS, as illustrated in Figure 94.1 The majority of cases of AS are acquired and result from degenerative (calcific) changes in an anatomically normal trileaflet aortic valve that becomes gradually dysfunctional over time Congenitally abnormal valves may be stenotic at birth but usually become dysfunctional during early adolescence or early adulthood A congenitally bicuspid aortic valve is now the most common course of valvular AS in patients under the age of 65 Rheumatic AS is now much less common than in prior decades and is virtually always accompanied by mitral valve disease Other forms of nonvalvular left ventricular outflow obstruction (e.g., discrete subvalve AS, hypertrophic cardiomyopathy, and supravalve AS) are discussed in other chapters The most reliable estimate of BAV prevalence is often considered to be the 1.37% reported by Larson and Edwards.4 The authors have a special expertise in aortic valve disease and amassed 21,417 consecutive autopsies with 293 BAVs An echocardiographic survey of primary school children demonstrated a BAV in 0.5% of males and 0.2% of females.8 A more recent study detected 0.8% BAVs in nearly 21,000 men in Italy who underwent echocardiographic screening for the military.9 Table 94.1 summarizes data on the prevalence of bicuspid valves Bicuspid aortic valve is seen predominantly in males, with a 2:1 male-to-female ratio.10–12 Although BAV may occur in isolation, it may also be associated with other congenital cardiovascular malformations, including coarctation, patent ductus arteriosus, supravalve AS, atrial septal defect, ventricular septal defect, sinus of Valsalva aneurysm, and coronary artery anomalies.1,13–16 There are also several syndromes in which BAV is a part of left-sided obstructive lesions of left ventricular inflow and outflow obstruction, including Shone syndrome (multiple left-sided lesions of inflow and outflow obstruction), Williams syndrome (supravalvular stenosis), and Turner syndrome (coarctation) Echocardiographic Features of Bicuspid Aortic Valves The roles of echocardiography in the detection and evaluation are listed in Box 94.3 The diagnosis of a BAV can usually be made by transthoracic echocardiography (TTE) When adequate images are obtained, sensitivities and specificities of up to 92% and 96%, respectively, have been reported for detecting BAV.22–24 The most reliable and useful views are the parasternal short-axis and longaxis views The echocardiographic features and their respective views are summarized in Box 94.3 The parasternal short-axis view (SAX) is extremely useful to examine the number and position of the commissures, the opening pattern, the presence of a raphe, and the leaflet mobility In contrast to the normal tricuspid aortic valve (TAV), which opens in a triangular fashion with straightening of the leaflets (see Fig 94.1; Fig 94.2, A), the BAV opens in an elliptical (“fish-mouth” or “football”) shape with curvilinear leaflets (see Fig 94.1; Figs 94.3 and 94.4) There is typically a raphe, a fibrous ridge that represents the region where the cusps failed to separate.10,25 The raphe is usually distinct and generally extends from 389 390 SECTION XV Aortic Stenosis TABLE 94.1 Prevalence of Bicuspid Aortic Valves (BAV) Box 94.1 Aortic Stenosis: Etiology Congenital (unicuspid, bicuspid, quadricuspid) Degenerative (sclerosis of previously normal valve) Rheumatic the free margins to the base of the leaflet Calcification commonly occurs first along this raphe, ultimately hindering the motion of the conjoined cusp.26 Rarely, the leaflets are symmetric and there is no raphe—a “pure” bicuspid valve Note that a false-negative diagnosis may occur when the raphe gives the appearance of a third coaptation line In diastole, the normal trileaflet aortic valve appears like a “Y” (inverted “Mercedes-Benz” sign), with the commissures at 10, 2, and o’clock (see Figs 94.1 and 94.2, B) When the commissures are deviated from those clock-face position, one should suspect a BAV and evaluate carefully An additional short-axis feature is a variable degree of leaflet redundancy In patients with very little redundancy of the leaflet margins, the development of stenosis is likely, whereas a significantly redundant leaflet with associated prolapse is more likely to lead to regurgitation The morphologic patterns of BAV vary according to which commissures have fused, and a number of classifications have been devised that pertain to the orientation of the leaflets1,10,27,28 (Fig 94.5, Table 94.2) Fusion of the right and left cusps is the most common morphologic type.28,29 In an echocardiographic study by Brandenburg and colleagues,23 the posterior commissure was located at or o’clock and the anterior commissure was located at or 10 o’clock when the valve is viewed in a parasternal shortaxis view The second most frequent type, fusion of the right and noncoronary cusps, has been linked to aortic arch involvement30–33 and may also be related to an increased risk of AS and regurgitation compared with the other anatomic types.29 The least common type is fusion of the left and noncoronary cusps.28 Michelena and colleagues similarly classified BAVs as typical (right-left coronary cusp fusion) if the commissures were at and 10 o’clock, and 11 o’clock, or to o’clock (anterior–posterior cusps) and atypical (right-noncoronary cusp fusion) if the commissures were at and o’clock or 12 and o’clock.19 Normal Rheumatic Author Year (n) BAV Prevalence Method Reference Wauchope Gross Larson and Edwards Datta et al Pauperio et al Basso et al Nistri et al 1928 1937 1984 9,996 5,000 21,417 0.5 0.56 1.37 Autopsy Autopsy Autopsy 1988 1999 8,800 2,000 0.59 0.65 Autopsy Autopsy 2004 2005 817 20,946 0.5 0.8 2D-echo 2D-echo Box 94.2 Complications of Bicuspid Aortic Valves Valve complications • Stenosis • Regurgitation • Infection (endocarditis) Aortic complications • Dilatation • Aneurysm • Dissection • Rupture Box 94.3 Bicuspid Aortic Valve: Role of Echocardiography • • • • • • Detection of bicuspid aortic valve Evaluation for aortic stenosis/regurgitation Careful measurements of aortic root and ascending aorta Search for coarctation Screening first-degree family members Surveillance—following valve dysfunction and aortopathy Calcific Bicuspid Figure 94.1 Diagram illustrating the diastolic (top row) and systolic (bottom row) appearances of a normal aortic valve and the three common etiologies of valvular aortic stenosis (Modified from Baumgartner H, Hung J, Bermejo J, et al Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice Eur J Echocardiogr 10:1–25, 2009.) Aortic Stenosis Morphology 391 94 A B Figure 94.2 Transthoracic echocardiogram (short-axis view) of a normal tricuspid aortic valve A, In diastole, the normal trileaflet valve appears like a “Y” with the commissures at 10, 2, and o’clock B, In systole, the valve opens in a triangular fashion with straightening of the leaflets n P P R L 270 (86%) R L 37 (12%) 315 P R L (3%) Figure 94.5 Variations in bicuspid valves Relative positions of raphe and conjoined cusp (Adapted from Sabet HY, Edwards WD, Tazelaar HD, et al Mayo Clin Proc 1999;74:14-26a) Figure 94.3 Transesophageal echocardiogram (cross section) of a bicuspid aortic valve that illustrates the elliptical (“fish-mouth” or “football”) shape with curvilinear leaflets in systole A B The parasternal long-axis (PLAX) view typically shows systolic doming (see Fig 94.4, B; and Fig 94.6) due to the limited valve opening In a normal TAV, the leaflets open parallel to the aortic walls In diastole, one of the leaflets (the larger, conjoined cusp) may prolapse The PLAX view with color Doppler is also useful to evaluate for aortic regurgitation (the diastolic aortic regurgitant jet is usually eccentric) and AS (turbulence in the aortic root and ascending aorta in systole) Last, the PLAX view is C Figure 94.4 Bicuspid aortic valve A, Short-axis view shows “fish-mouth” or football-shaped opening B, Long-axis view shows systolic doming C, Color Doppler shows eccentric aortic regurgitant jet (typical of bicuspid aortic valve) 392 SECTION XV Aortic Stenosis TABLE 94.2 Distinctive Echocardiographic Features of Bicuspid Aortic Valves View Systolic doming Eccentric valve closure Single commissural line in diastole Two cusps, two commissures Raphe Oval opening (football-shaped; fish-mouth, elliptical; “CBS-eye”) Unequal cusp size PLAX PLAX SAX SAX SAX SAX PLAX, SAX PLAX, Parasternal long-axis; SAX, parasternal short-axis Figure 94.7 M-mode echocardiogram (echo) and phonocardiogram (phono) from a patient with a bicuspid aortic valve The echo illustrates an eccentric closure line (green arrows) in both late and early diastolic; the phono illustrates an aortic ejection sound (indicated by the bottom of the red arrow) that occurs at the maximal abrupt opening of the aortic valve (indicated by the red arrowhead) consequently the jet flow may be abnormal in its direction.31 Hope and colleagues32 demonstrated two different flow patterns that were specific to the two most common cusp fusion types Fusion of the right-left coronary cusps generated a right-anterior flow jet, whereas fusion of the right-noncoronary cusps generated a left-posterior flow jet Figure 94.6 Transesophageal echocardiographic longitudinal view of the aortic root and ascending aorta illustrating the systolic doming of a bicuspid aortic valve also important for sizing the sinus of Valsalva, sinotubular junction, and ascending aorta With increasing age, as the leaflets become thickened, fibrotic, and calcified, systolic doming may no longer be evident and the typical short-axis appearance of the BAV may be difficult to distinguish from calcific AS of a TAV In fact, there is an inverse association between the degree of valve stenosis and accuracy of echocardiographically determined valve structure and etiology.34 The elliptical systolic opening in the SAX view is not easily appreciated in a severely stenotic valve M-mode echo of a BAV may demonstrate an eccentric closure line (Fig 94.7), but this sign is not reliable, and approximately 25% of patients with a BAV have a relatively central closure line Moreover, occasionally TAVs can also appear to have an eccentric closure line depending on image quality and orientation of the echo beam If images are suboptimal or heavily fibrotic/sclerotic, then transesophageal echocardiography (TEE) may improve visualization of the leaflets and may be helpful for accurate evaluation of the aortic valve anatomy and confirmation of a BAV In some instances, alternative cardiac imaging, such as computed tomography (CT) or magnetic resonance imaging (MRI), may help confirm BAV anatomy More commonly, these imaging modalities are used to visualize the thoracic aorta Recently, phase contrast MRI has demonstrated abnormal flow patterns in the ascending aorta in patients with a BAV, with or without stenosis or aneurysm.32 Even if the valve orifice is not reduced (i.e., no stenosis), it is geometrically altered in BAV, and Coarctation Bicuspid aortic valve may occur in isolation or in association with other forms of congenital heart disease There is a well-documented association of BAV with coarctation.7,20,24,35–40 An autopsy study found coexisting coarctation of the aorta in 6% of cases of BAV,1 and an echocardiographic study found coarctation in 10% of patients with BAV.38 On the other hand, as many as 30% to 70% of patients with coarctation have a BAV.* Therefore, when a BAV is detected on an echocardiogram, coarctation of the aorta should always be sought Infective Endocarditis Patients with BAVs are particularly susceptible to infective endocarditis Although the exact incidence of endocarditis remains controversial, the population risk, even in the presence of a functionally normal valve, may be as high as 3% over time.1 The estimated incidence is 0.16% per year in unoperated children and adolescents.41 In adults, the two large case series by Tzemos and Michelena and their colleagues18,19 suggest that the incidence is 0.3% and 2% per year, respectively In a series of 128 microbiologically proven episodes of endocarditis, the commonest predisposing risk factor was BAV (16.7%).42 In another series of 50 patients with native valve endocarditis, 12% had BAV.43 In many cases of BAV, endocarditis is the first indication of structural heart disease This fact emphasizes the importance of either clinical or echocardiographic screening for the diagnosis of BAV Unexplained systolic ejection sounds (clicks) should prompt echocardiographic evaluation Surprisingly, bacterial endocarditis prevention is no longer recommended by the most recent *References 7, 20, 29, 37, 40 Aortic Stenosis Morphology 393 TABLE 94.3 Frequency of Aortic Dissection in Persons with a Bicuspid Aortic Valve (BAV) Author(s) Year Frequency of Aortic Dissection in BAV Fenoglio Larsen and Edwards Roberts and Roberts Michelena et al 1977 1984 1991 2011 8/152 (5%) 18/293 (6%) 14/328 (4%) 2/416 (0.4%) 94 Population Reference Autopsy, !20 years old Autopsy, all ages Autopsy, >15 years old Echocardiography by population-based community cohort 99 100 19 American College of Cardiology/American Heart Association (ACC/AHA) Guideline for BAV.44 Aortic Complications Bicuspid aortic valve is associated with several additional abnormalities, including displaced coronary ostia, left coronary artery dominance, and a shortened left main coronary artery; coarctation of the aorta; aortic interruption; Williams syndrome; and, most importantly, aortic dilatation, aneurysm, and dissection Given these collective findings, it can be suggested that BAV is the result of a developmental disorder involving the entire aortic root and arch Although the pathogenesis is not well understood, these associated aortic malformations suggest a genetic defect.14 Although less well understood, these aortic complications of BAV disease can cause significant morbidity and mortality As listed in Box 94.2, BAV may be associated with progressive dilatation, aneurysmal formation, and dissection (Tables 94.3 and 94.4) These vascular complications may occur independent of valvular dysfunction* and can manifest in patients without significant stenosis or regurgitation According to Nistri and colleagues, 50% or more of young patients with normally functioning bicuspid aortic valves have echocardiographic evidence of aortic dilatation.9 Therefore, the size and shape of the aortic root and dimensions should be carefully evaluated and followed serially Aortic root dimensions should be performed at the level of the annulus, sinuses of Valsalva, sinotubular junction (STJ), and proximal ascending aorta (Fig 94.8) In BAV (unlike Marfan syndrome, where the dilation is usually more pronounced at the sinus level), the sinuses are usually normal or mildly dilated and the aortic dilation is often most pronounced in the ascending aorta distal to the STJ48,49 (Figs 94.9 and 94.10) Therefore, effort should be made to image this portion of the aorta The midportion of the ascending aorta may not be easily imaged with echocardiography, and evaluation with CT or MRI may be required.50 The aortic arch and descending thoracic aorta may also become dilated Recently, it has been reported that patients with BAV are also at increased risk for intracranial aneurysms compared with the general population.51 LV Ao LA Figure 94.8 Diagram of a parasternal long-axis view illustrating where aortic dimension measurements should be made: 1, aortic annulus; 2, midpoint of sinuses of Valsalva level; 3, sinotubular junction level; 4, mid-ascending aorta Measurements should be made perpendicular to the long axis of the aorta Ao, Aortic root; LA, left atrium; LV, left ventricle TABLE 94.4 Frequency of Bicuspid Aortic Valve (BAV) in Aortic Dissection (Spontaneous, Noniatrogenic Dissection at Autopsy) Author(s) Year Number BAV/Dissection Reference Gore and Seiwert Edwards Larson and Edwards Roberts and Roberts Totals 1952 1978 1984 11/85 13% 11/119 9% 18/161 11% 101 102 1991 14/186 7.5% 100 54/551 ¼ 10% *References 9, 11, 15, 46, 47 Figure 94.9 A diagram of a thoracic aorta illustrating the most common type of aortopathy associated with bicuspid aortic valves—normal aortic root with dilatation beginning at/above the sinotubular junction Although BAV aortopathy may share similarities with the Marfan syndrome, and aortic aneurysms are common in both conditions, a recent retrospective cohort study of 416 consecutive patients with definite BAV provides evidence that their clinical outcomes are different and that aortic dissection is more common in Marfan syndrome.18 The risk of aortic dissection in this BAV 394 SECTION XV Aortic Stenosis Unicuspid Aortic Valve Asc’g Ao Figure 94.10 Transesophageal echocardiographic longitudinal view that shows a markedly dilated ascending aorta (Asc’g Ao) that spares the aortic root—typical type of aortopathy associated with bicuspid aortic valve Other less common congenital abnormalities of the aortic valve include the unicuspid valve and quadricuspid valve The unicuspid aortic valve (UAV) is a rare congenital malformation seen in approximately 0.002% of patients referred for echocardiography, but in as many as 4% to 6% of patients undergoing surgery for “pure” (isolated) AS.55 Two forms of UAV are recognized: One has no commissures or lateral attachments to the aorta at the level of the orifice (acommissural), and the second has one lateral attachment to the aorta at the level of the orifice (unicommissural).56 Both of these types, like the BAV, produce a dome-shaped opening in systole57 (Fig 94.11) The latter is the more common of the two AS of an acommissural UAV is quite severe, presents in infancy, and is seldom, if ever, seen in adults.58 An acommissural type of UAV has a central round, oval, or triangular opening caused by underdevelopment of all three cusps, resulting in a “volcano-like” structure with a small, central orifice (Fig 94.12, A) Stenosis of an acommissural valve is typically very severe and occurs during infancy In a unicommissural type of UAV, there is usually an eccentric “teardrop”-shaped opening (see Fig 94.12, B) The most common position of the single commissural attachment zone in this type is posterior59 (Video 94.1) This configuration results in a relatively larger orifice than the acommissural type As a result, some patients with a unicommissural UAV live into adulthood before manifesting valvular obstruction Like BAV patients, UAV patients are more often male.59 Compared with patients undergoing surgery Acommissural Unicommissural cohort was approximately times higher than in the general population, but despite the high relative risk, the absolute incidence of aortic dissection was very low (given the BAV prevalence of 1.3% of the general population).17 Surveillance (Serial Assessment of Patients with Bicuspid Aortic Valve) Because of the risk of progressive aortic valve disease (stenosis and/or regurgitation) and aortopathy, all BAV patients should undergo annual imaging, even when asymptomatic The 2008 focused update of the 2006 ACC/AHA guidelines recommended monitoring adolescents and young adults, older patients with AS, and patients with a BAV and dilation of the aortic root and/or ascending aorta.52 TTE can be used for serial imaging follow-up of the ascending aorta when the dimensions measured by TTE and CT or MRI have been confirmed Following identification of ascending aortic enlargement in a patient with BAV, repeat imaging at months is recommended If the aorta remains stable at months and is less than 45 mm in size, and if there is no family history of aortic dissection, annual imaging is recommended Patients who not meet these criteria should have repeat aortic imaging with TTE every months If the aortic root is poorly visualized on echocardiography, cardiac CT or MRI are excellent substitutes TEE is generally not used for serial follow-up of BAV-related aortopathy because of its semi-invasive nature and the difficulty of comparing dimensions over time Anterior mitral leaflet Dome (“volcano,” no lateral attachments) (“Exclamation point” one lateral attachment) Figure 94.11 Diagram of the two types of unicuspid aortic valves (see text) Family Screening of Patients with BAV BAV appears inheritable and was present in 9.1% of first-degree relatives in one study.38 Although the current ACC/AHA guidelines on valve disease52 not recommend screening for relatives of individuals with BAV, the ACC/AHA guidelines on congenital heart disease53 and thoracic aortic disease54 recommended echocardiographic screening of first-degree relatives (class I; level of evidence C) A B Figure 94.12 Diagram illustrating the two types of unicuspid aortic valves A, Unicommissural valve has a teardrop opening and a lateral attachment B, Acommissural valve illustrating a central round/oval opening at the top of a conical or dome-shaped valve Aortic Stenosis Morphology for BAV and TAV disease, unicommissural UAV patients present about decades earlier than patients with BAV60 and decades earlier than patients with TAV.61 Unicommissural UAV patients usually require surgery in the third decade of life In a UAV, the coronary arteries are generally in the normal position.58 Aortopathy similar to that seen with a BAV may be present.56 Unicuspid aortic valves usually have severe, diffuse calcification, and distinguishing a UAV from a BAV can be challenging (see Fig 94.12) TEE is more accurate for making this distinction.56,62,63 Quadricuspid Aortic Valve Quadricuspid aortic valve (QAV) is a rare congenital cardiac abnormality with a prevalence that ranges from 0.008% to 0.043%, according to autopsy and echocardiography series (Table 94.5).64,65 A much higher incidence was reported by Olson and colleagues in a review of 225 patients undergoing surgery for pure aortic regurgitation.66 Most cases historically were discovered incidentally at surgery or postmortem examination However, the majority of cases are now diagnosed antemortem by echocardiography.67,68 Because of further advances in imaging, including TEE, CT, and MRI, more cases are being detected, which is likely to alter the incidence of QAV.69–71 Based on the relative size of the cusps and their equality, Hurwitz and Roberts delineated seven morphologic subtypes of QAV (types A through G), ranging from four cusps of equal size to four unequal cusps.72 The most common configuration appears to be that of four equal or nearly equal cusps (Table 94.6).72–74 The QAV may function normally—most commonly when the cusps are relatively equal in size.64,73 In general, valve dysfunction is seldom present or minimal during childhood or adolescence.64,65,72,75 Aortic valve dysfunction is usually due to aortic regurgitation (Table 94.7) and tends to occur later in life, a 395 TABLE 94.7 Function of Quadricuspid Aortic Valves Valve Function N % AR AS + AR AS Normal 115 13 25 75% 8% 1% 16% From Tutarel, J Heart Valve Dis 13:534-537, 2004 (Reference 67) consequence of progressive leaflet thickening with resultant incomplete coaptation (Video 94.2) Unlike BAV, the association of ascending aortic aneurysm is extremely rare The characteristic echocardiographic finding is an “X”-shaped pattern in diastole in short-axis views (formed by the commissural lines of the closed QAV), compared with the “Y” in normal trileaflet valves (Fig 94.13) Because valve dysfunction may occur with advancing age, clinical and echocardiographic follow-up is recommended Although QAV is usually an isolated anomaly,64,72,73 various cardiac and noncardiac anomalies have been reported in association with it (Box 94.4).76–78 The most prevalent cardiac malformations associated with QAV are coronary artery anomalies, which have been reported in 10% of cases.67,79–83 In summary, QAV is a rare congenital disorder, usually diagnosed in adulthood, with a potential for complications—mainly aortic regurgitation QAVs often require surgery, usually in the fifth and sixth decades, and therefore need close follow-up TABLE 94.5 Quadricuspid Aortic Valve—Prevalence Author Year Method n % Ref Simonds Simonds 1923 1923 0/2000 2/25,666 Feldman et al Feldman et al Olson et al 1990* 1990† 1984 Autopsy Autopsy (literature review) 2D-echo 2D-echo Surgery for pure AR 0.000% 0.008% 0.013% 0.043% 1% 64 64 65 66 66 8/60,446 6/13,805 2/225 AR, Aortic regurgitation *1982-1988 † 1987-1988 Figure 94.13 Quadricuspid aortic valve Transesophageal echocardiographic short-axis view (37 degrees) illustrates failure of leaflet coaptation in diastole (arrow) with a square central opening and typical X-shaped configuration of the four commissures TABLE 94.6 Quadricuspid Aortic Valves: Morphologic Types Anatomic Variation—Cusps N equal equal, smaller equal larger and equal smaller large, intermediate, small equal and larger equal, unequal smaller unequal 51 43 10 4 From Hurwitz LE, Roberts WC: Quadricuspid semilunar valve, Am J Cardiol 31:623-626, 1973 (Reference 72) Box 94.4 Cardiac and Noncardiac Abnormalities Associated with Quadricuspid Valve Patent ductus arteriosus Hypertrophic cardiomyopathy Subaortic stenosis Ehlers-Danlos syndrome Coronary ostium displacement Ventricular septal defect 94 396 SECTION XV Aortic Stenosis CALCIFIC (DEGENERATIVE) AORTIC STENOSIS Calcific AS is the most common etiology of valvular AS in elderly patients The prevalence of calcific AS increases with age.84 AS has a prevalence of about 5% in individuals age 65 or older and about 10% in individuals age 80 years or older AS is the most common indication for valve replacement surgery and the second most common indication for surgery in older adults, surpassed only by coronary artery bypass grafting.85 Calcific AS affects men and women equally Because the prevalence of AS increases with age and because calcification occurs in regions of mechanical stress, AS was previously thought to be a degenerative disorder caused by passive “wear and tear.” However, the view that aortic valve calcification is a passive consequence of cellular aging has been challenged AS is now considered to be an active process with some similarities to atherosclerosis, including inflammation, lipid infiltration, and dystrophic calcification.86–90 Therefore, the term calcific AS seems more appropriate than degenerative AS Currently, the pathology of calcific aortic valve disease is an area of active research.91,92 Calcific AS results from slowly progressing fibrosis and calcification, which occurs over several decades, leading to variable degrees of thickening and rigidity of the aortic valve cusps This process begins with aortic valve sclerosis that does not limit flow through the aortic orifice The morphologic hallmark is the formation of calcified masses along the aortic side of the cups The earliest deposits occur at the cusp attachments and along the line of cusp coaptation—the sites of greatest bending and unbending during valve opening and closing.93 Irregular leaflet thickening and focal increased echogenicity (calcifications) are the echocardiographic hallmarks of calcific AS These focal areas of thickening are Stenotic unicuspid AV typically seen in the center of the valve cusps The degree of calcification is best assessed in the parasternal short-axis view The degree of calcification can be qualitatively classified as mild (small isolated spots or nodules), moderate (multiple larger nodules), and severe (extensive thickening and calcification of all of the cusps).89,94 The degree of leaflet calcification is a marker of disease progression and should be reported.94,95 As the leaflets become more sclerotic, they become progressively more rigid and less mobile and begin to obstruct flow Increases in aortic transvalvular flow velocity mark the progression from aortic sclerosis to AS In the most severe cases, the aortic root appears to be filled with dense, amorphous echoes that have little or no motion In some patients, one of the leaflets may become immobile while the others move freely When only one leaflet is immobile, there is usually only a mild increase in transaortic velocity (mild AS) Unlike rheumatic AS, commissural fusion is usually absent or only minimal in calcific AS The valve orifice tends to be triradiate—three slitlike openings in systole (Figs 94.14, E and 94.15).96 Calcification often extends onto the base of the anterior mitral leaflet Calcification may also extend from the valve cusps into the ventricular septum and may induce conduction abnormalities RHEUMATIC AORTIC STENOSIS Rheumatic AS has become uncommon in the developed world, although it remains a significant cause of AS worldwide In adults undergoing aortic valve replacement for symptomatic AS in the United States, calcific tricuspid AS accounts for 5% of cases, bicuspid AS for 36%, and rheumatic AS for 9%.97 Aortic rheumatic valve disease is never isolated, but is virtually always associated with Stenotic bicuspid AV A C B D Stenotic tricuspid AV E Figure 94.14 Gross pathology specimens of stenotic aortic valves (AVs), including unicuspid, bicuspid, and tricuspid valves The two unicuspid AVs (A and B) are unicommissural with lateral attachments; the two bicuspid valves (C and D) have raphes (arrows); tricuspid valve (E) does not have fused commissures and shows the slitlike orifices resulting from bulky calcific deposits that restrict leaflet motion (Courtesy of Dr Renu Virmani, CVPath Institute, Gaithersburg, Md.) Aortic Stenosis Morphology Figure 94.15 Gross pathology specimen of a calcific (degenerative) trileaflet aortic valve that illustrates absence of commissural fusion and a triradiate orifice, each of which are slitlike (Courtesy of Dr Renu Virmani, CVPath Institute, Gaithersburg, Md.) 397 rheumatic mitral valve disease Rheumatic valvular dysfunction may affect not only an anatomically normal TAV, but also a congenital BAV Similar to rheumatic mitral valve disease, rheumatic aortic valve deformities are characterized by diffuse cuspal thickening that extends to their free edges and by commissural fusion These features contrast with the morphologic features of degenerative (calcific) AS, which manifests basal calcific nodules, minimal or no involvement of the free edges, and no commissural fusion The acquired commissural fusion in rheumatic AS may affect one, two, or all three commissures and is usually distinguishable from the commissural fusion of congenital valve abnormalities The commissural fusion, which begins at the annulus and progresses toward the center, often affects each commissure equally, producing a small, central, circular or triangular orifice (see Fig 94.1; Fig 94.16) Subsequent calcium deposition occurs secondarily Commissural fusion is the primary lesion of AS, as opposed to fibrosis/sclerosis, shortening, and retraction of the cusps, which produce rheumatic aortic regurgitation Interestingly, the sole pathognomonic feature of rheumatic valve disease, the Aschoff granuloma, is virtually never found in aortic valve tissue.98 Please access ExpertConsult to see Videos 94.1 and 94.2 REFERENCES A B Figure 94.16 A, Typical rheumatic aortic stenosis with commissural fusion resulting in a central triangular (as shown here) or oval or circular (not shown) orifice as shown in the transesophageal echocardiogram B, A pathologic specimen from a different patient Roberts WC: The congenitally bicuspid aortic valve A study of 85 autopsy cases, Am J Cardiol 26:72–83, 1970 Wauchope GM: The clinical importance of variations in the number of cusps forming the aortic and pulmonary valves, Q J Med 21:383–399, 1928 Gross L: So-called congenital bicuspid aortic valve, Arch Pathol 23:350–362, 1937 Larson EW, Edwards WD: Risk factors for aortic dissection: a necropsy study of 161 cases, Am J Cardiol 53:849–855, 1984 Datta BN, Bhusnurmah B, Khatri HN, et al.: Anatomically isolated aortic valve disease Morphologic study of 100 cases at autopsy, Jpn Heart J 29:661–670, 1988 Pauperio HM, Azevedo AC, Ferreira C: The aortic valve with two leaflets A study in 2000 autopsies, Cardiol Young 9:488–498, 1999 Ward C: Clinical significance of the bicuspid aortic valve, Heart 83:81–85, 2000 Basso C, Boschello M, Perrone C, et al.: An echocardiographic survey of primary school children for bicuspid aortic valve, Am J Cardiol 93:661–663, 2004 Nistri S, Basso C, Marzari C, et al.: Frequency of bicuspid aortic valve in young male conscripts by echocardiogram, Am J Cardiol 96:718–721, 2005 10 Sabet HY, Edwards WD, Tazelaar HD, et al.: Congenital bicuspid aortic valves: a surgical pathology study of 542 cases and a literature review of 2,715 additional cases, Mayo Clin Proc 74:14–26, 1999 11 Keane MG, Wiegers SE, Plappert T, et al.: Bicuspid aortic valves are associated with dilatation out of proportion to coexistent valvular lesions, Circulation 102 (Suppl III):III 35–III 39, 2000 12 Chan KL, Ghani M, Woodend K, et al.: Case-controlled study to assess risk factors for aortic stenosis in congenitally bicuspid aortic valve, Am J Cardiol 88:690–693, 2001 13 Jureidini SB, Singh GK, Marino CJ, et al.: Aberrant origin of the left coronary artery from the right aortic sinus: surgical intervention based on echocardiographic diagnosis, J Am Soc Echocardiogr 13:1117–1120, 2000 14 Fedak PW, Verma S, David TE, et al.: Clinical and pathophysiological implications of a bicuspid aortic valve, Circulation 106:900–904, 2002 15 Doty DB: Anomalous origin of the left circumflex coronary artery association with bicuspid aortic valve, J Thorac Cardiovasc Surg 122:842–843, 2001 16 Ko SM, Song MG, Hwang HK: Bicuspid aortic valve: spectrum of imaging findings at cardiac MDCT and cardiovascular MRI, AJR Am J Roentgenol 198:89–97, 2012 17 Michelena HI, Desjardins VA, Avierinos JF, et al.: Natural history of asymptomatic patients with normally functioning or minimally dysfunctional bicuspid aortic valve in the community, Circulation 117:2776–2784, 2008 18 Tzemos N, Therrien J, Yip J, et al.: Outcomes in adults with bicuspid aortic valve, JAMA 300:1317–1325, 2008 19 Michelena HI, Khanna AD, Mahoney D, et al.: Incidence of aortic complications in patients with bicuspid aortic valves, JAMA 306:1104–1113, 2011 20 Siu SC, Silversilles CK: Bicuspid aortic valve disease, J Am Coll Cardiol 55:2789–2800, 2010 21 Roberts WC, Ko JM, Matter GJ: Isolated aortic valve replacement without coronary bypass for aortic valve stenosis involving a congenitally bicuspid valve in a nonagenarian, Am Geriatr Cardiol 15:389–391, 2006 22 Zema MJ, Caccavano M: Two-dimensional echocardiographic assessment of aortic valve morphology: feasibility of bicuspid aortic valve detection Prospective study of 100 adult patients, Br Heart J 48:428–433, 1982 94 398 SECTION XV Aortic Stenosis 23 Brandenburg RO, Tajik AJ, Edwards WD, et al.: Accuracy of dimensional echocardiographic diagnosis of congenitally bicuspid aortic valve: echocardiographicanatomic correlation in 115 patients, Am J Cardiol 51:1469–1473, 1983 24 Chan KL, Stinson WA, Veinot JP: Reliability of transthoracic echocardiography in the assessment of aortic valve morphology: pathological correlations in 178 patients, Can J Cardiol 15:48–52, 1999 25 Pomerance A: Pathogenesis of aortic stenosis and its relation to age, Br Heart J 334:569–574, 1972 26 Waller BF, Carter JB, Williams Jr HJ, et al.: Bicuspid aortic valve Comparison of congenital and acquired types, Circulation 48:1140–1150, 1973 27 Angelini A, Ho SY, Anderson RH, et al.: The morphology of the normal aortic valve as compared with the aortic valve having leaflets, J Thorac Cardiovasc Surg 98:362–367, 1989 28 Sievers HH, Schmidtke C: A classification system for the bicuspid aortic valve from 304 surgical specimens, J Thorac Cardiovasc Surg 133:1226–1233, 2007 29 Fernandes SM, Sanders SP, Khairy P, et al.: Morphology of bicuspid aortic valve in children and adolescents, J Am Coll Cardiol 44:1648–1651, 2004 30 Schaefer BM, Lewin MB, Stout KK, et al.: The bicuspid aortic valve: an integrated phenotypic classification of leaflet morphology and aortic root shape, Heart 94:1634–1638, 2008 31 Della Corte A, Cortufo M: Bicuspid aortopathy or bicuspid aortopathies? The risk in generalizing, J Thorac Cardiovasc Surg 136:1604, 2008 32 Hope MD, Meadows AK, Hope TA, et al.: Evaluation of bicuspid aortic valve and aortic coarctation with 4D flow magnetic resonance imaging, Circulation 117:2818–2819, 2008 33 Giradauskas E, Borger MA, Secknus MA, et al.: Is aortopathy in bicuspid aortic valve disease a congenital defect or a result of abnormal hemodynamics? A critical appraisal of one-sided argument, Eur J Cardiothorac Surg 39:809–814, 2011 34 Ayad RF, Grayburn PA, Ko JM, et al.: Accuracy of two-dimensional echocardiography in determining aortic valve structure in patients > 50 years of age having aortic valve replacement for aortic stenosis, Am J Cardiol 108:1589–1599, 2011 35 Litherson RR, Pennington DG, Jacobs ML, et al.: Coarctation of the aorta: review of 234 patients and clarification of management problem, Am J Cardiol 43:835–840, 1979 36 Folger GM Jr, Stein PD: Bicuspid aortic valve morphology associated with coarctation of the aorta, Cathet Cardiovasc Diagn 10:17–25, 1984 37 Nihoyannopoulos P, Karas S, Sapsford RN, et al.: Accuracy of two-dimensional echocardiography in the diagnosis of aortic arch obstruction, J Am Coll Cardiol 10:1072–1077, 1987 38 Huntington K, Hunter A, Chan K: A prospective study to assess the frequency of familial clustering of congenital bicuspid aortic valve, J Am Coll Cardiol 30:1809–1812, 1997 39 Warnes CA: Bicuspid aortic valve and coarctation: two villains part of a diffuse problem, Heart 89:965–966, 2003 40 Oliver JM, Gallego P, Gonzalez A, et al.: Risk factors for aortic complications in adults with coarctation of the aorta, J Am Coll Cardiol 44:1641–1647, 2004 41 Gersony WM, Hayes CJ, Driscoll DJ, et al.: Bacterial endocarditis in patients with aortic stenosis Pulmonary stenosis, or ventricular septal defect, Circulation 87 (Suppl 2):I 121–I 126, 1993 42 Dyson C, Barnes RA, Harrison GA: Infective endocarditis: an epidemiological review of 128 episodes, J Infect 38:87–93, 1999 43 Lamas CC, Eykyn SJ: Bicuspid aortic valve—a silent danger: analysis of 50 cases of infective endocarditis, Clin Infect Dis 30:336–341, 2000 44 Wilson W, Taubert KA, Gewitz M, et al.: Prevention of infective endocarditis: a guideline from the American Heart Association, Circulation 116:1736–1754, 2007 45 Niwa K, Perloff JK, Bhuta SM, et al.: Structural abnormalities of great arterial walls in congenital heart disease: light and electron microscopic analyses, Circulation 103:393–400, 2001 46 Ferencik M, Pape LA: Changes in size of ascending aorta and aortic valve function with time in patients with congenitally bicuspid aortic valves, Am J Cardiol 92:43–46, 2003 47 Plaisance BR, Winkler MA, Attili AK, et al.: Congenital aortic valve first presenting as an aortic aneurysm, Am J Med 125:e5–e7, 2012 48 Della Corte A, Bancone C, Quarto C, et al.: Predictors of ascending aortic dilatation with bicuspid aortic valve: a wide spectrum of disease expression, Eur J Cardiothorac Surg 31:397–404, 2007 49 Braverman AC: Aortic involvement in patients with a bicuspid aortic valve, Heart 97:506–513, 2011 50 Isselbacher EM: Thoracic and abdominal aortic aneurysms, Circulation 111:816–828, 2005 51 Schievink WI, Raissi SG, Maya MM, et al.: Screening for intracranial aneurysms in patients with bicuspid aortic valve, Neurology 74:1430–1433, 2010 52 Bonow RO, Carabello BA, Chatterjee K, et al.: 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease, Circulation 118:e523–e564, 2008 53 Warnes CA, Williams RG, Bashore TM, et al.:ACC/AHA 2008 guidelines for themanagement of adults with congenital heart disease, Circulation 118(1):e714–e833, 2008 54 Hiratzka LF, Bakris GL, Beckman JA, et al.: 2010 ACCF/AHA/AATS/ACR/ SCA/SCAI/SIR/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease, Circulation 121:e266–e369, 2010 55 Roberts WC, Ko JM: Frequency by decades of unicuspid, bicuspid, and tricuspid aortic valves in adults having isolated aortic valve replacement for aortic stenosis, with or without associated aortic regurgitation, Circulation 111:920–925, 2005 56 Tempe DK, Garg M, Tower AS, et al.: Unicuspid aortic valve: transesophageal echocardiographic features, J Cardiothorac Vasc Anesth 26:277–279, 2012 57 Osman K, Nanda NC, Kim K-S, et al.: Transesophageal echocardiographic features of a unicuspid aortic valve, Echocardiography l1:469–473, 1994 58 Sniecinski RM, Shanewisc JS, Glas KE: Transesophageal echocardiography of a unicuspid aortic valve, Anesth Analg 108:788–789, 2009 59 Novaro GM, Tiong IY, Pearce GL, et al.: Features and predictors of ascending aortic dilatation in association with a congenital bicuspid aortic valve, Am J Cardiol 92:99–101, 2003 60 Yotsumoto G, Moriyama Y, Toyohira H, et al.: Congenital bicuspid aortic valve: analysis of 63 surgical cases, J Heart Valve Dis 7:500–503, 1998 61 Passik CS, Ackerman DM, Pluth JR, et al.: Temporal changes in the cases of aortic stenosis: a surgical pathology study of 646 cases, Mayo Clin Proc 62:119–123, 1987 62 Chu JW, Picard MH, Agnihotri AK, et al.: Diagnosis of congenitally unicuspid aortic valve in adult population: the value and limitation of transesophageal echocardiography, Echocardiography 27:1107–1112, 2010 63 Brantley HP, Nekkanti R, Anderson CA, et al.: Three-dimensional echocardiographic features of unicuspid aortic valve stenosis correlate with surgical findings, Echocardiography 29:E204–E207, 2012 64 Simonds JP: Congenital malformation of the aortic and pulmonary valves, Am J Med Sci 166:584–595, 1923 65 Feldman BJ, Khandheria BK, Warnes CA, et al.: Incidence description, and functional assessment of isolated quadricuspid aortic valves, Am J Cardiol 65:937–938, 1990 66 Olson LJ, Subramannian MB, Edwards WD: Surgical pathology of pure aortic insufficiency: a study of 725 cases, Mayo Clin Proc 59:835–841, 1984 67 Tutarel O: The quadricuspid aortic valve: a comprehensive review, J Heart Valve Dis 13:534–537, 2004 68 Zacharaki AA, Patrianakos AP, Parthenakos FI, et al.: Quadricuspid aortic valve associated with non-obstructive sub-aortic membrane: a case report and review of the literature, Hellenic J Cardiol 50:544–547, 2009 69 Gulati A, Chan C, Viertel A, et al.: Quadricuspid aortic valve: the four-leaf clover discovered by cardiac MRI, J Heart Valve Dis 18:583–584, 2009 70 Hunt GB: Congenital quadricuspid aortic valve detected on chest CT, J Med Imaging Radiol Oncol 53:380–381, 2009 71 Chapman CB, Kohmoto T, Kelly AF, et al.: Cardiac computed tomography and quadricuspid aortic valve: a case report, WMJ 109:219–221, 2010 72 Hurwitz LE, Roberts WC: Quadricuspid semilunar valve, Am J Cardiol 31:623–626, 1973 73 Davia JE, Fenoglio JJ, De Castro CM, et al.: Quadricuspid semilunar valves, Chest 72:186–189, 1977 74 Barbosa MM, Motta MS: Quadricuspid aortic valve and aortic regurgitation diagnosed by Doppler echocardiography Report of two cases and a review of the literature, J Am Soc Echocardiogr 4:69–74, 1991 75 Peretz DI, Changfoot GH, Gourlay RH: Four-cusped aortic valve with significant insufficiency, Am J Cardiol 23:291–293, 1969 76 Janssens U, Klues HG, Hanrath P: Congenital quadricuspid aortic valve anomaly associated with hypertrophic nonobstructive cardiomyopathy: a case report and review of the literature, Heart 78:83–87, 1997 77 Brouwer MHJ, de Graaf JJ, Ebels T: Congenital quadricuspid aortic valve, Int J Cardiol 38:196–198, 1993 78 Dotti MT, De Stefano N, Mondillo S, et al.: Neurological involvement and quadricuspid aortic valve in a patient with Ehlers-Danlos syndrome [letter], J Neurol 246:612–613, 1999 79 Robicsek F, Sanger PW, Daughtery HK, et al.: Congenital quadricuspid aortic valve with displacement of the left coronary orifice, Am J Cardiol 23:288–290, 1969 80 Korosawa H, Wagenaar SS, Becker AZ: Sudden-death in a youth A case of quadricuspid aortic valve with isolation of original left coronary artery, Br Heart J 46:211–215, 1981 81 Rosenkranz ER, Murphy DJ Jr, Cosgrove DM 3rd: Surgical management of left coronary ostial atresia and supravalvular aortic stenosis, Am Thorac Surg 94:779–781, 1992 82 Lanzillo G, Breccia PA, Intonti F: Congenital quadricuspid aortic valve with displacement of the right coronary orifice, Scand J Thorac Cardiovasc Surg 15:149–151, 1981 83 Okmen AS, Okmen E: Quadricuspid aortic valve without severe dysfunction despite advanced age, Tex Heart Inst J 36:486–488, 2009 84 Lindroos M, Kupari M, Heikkila J, et al.: Prevalence of aortic valve abnormalities in the elderly: an echocardiographic study of a random population sample, J Am Coll Cardiol 21:1220–1225, 1993 85 Rajamannan NM, Bonow RO, Rahimtoola SH: Calcific aortic stenosis: an update, Nat Clin Pract Cardiovasc Med 4:254–262, 2007 86 Stewart BF, Siscovick D, Lind BK, et al.: Clinical factors associated with calcific aortic valve disease: Cardiovascular Health Study, J Am Coll Cardiol 29:630–634, 1997 87 Agmon Y, Khandheria BK, Meissner I, et al.: Aortic valve sclerosis and aortic atherosclerosis: different manifestations of the same disease? Insights from a population-based study, J Am Coll Cardiol 38:827–834, 2001 88 O’Brien KD: Pathogenesis of calcific aortic valve disease: a disease process comes of age (and a great deal more), Arterioscler Thromb Vasc Biol 26:1721–1728, 2006 89 Otto CM: Calcific aortic stenosis—time to look more closely at the valve, N Engl J Med 359:1395–1398, 2008 90 Owens DS, Katz R, Takasu J, et al.: Incidence and progression of aortic valve calcium in the Multi-Ethnic Study of Atherosclerosis (MESA), Am J Cardiol 105:701–708, 2010 91 Owens DS, Otto CM: Is it time for a new paradigm in calcific aortic valve disease? JACC Cardiovasc Imaging 2:928–930, 2009 Index H Hand-held echocardiography, 85–89 Hand-carried cardiac ultrasound, 85 background of, 85 color Doppler and, 85 instrumentation of, 85, 86f spectral Doppler and, 85 technique in, 85–87, 86f, 87b Handgrip, exercise stress echocardiography and, 247 HCM See Hypertrophic cardiomyopathy (HCM) Health-care associated infective endocarditis, 577 Heart athletic, 295, 296f, 319 right, echocardiographic evaluation of, 386, 387f systemic diseases, 797 univentricular, 727 Heart disease, pulmonary, 381 Heart failure infective endocarditis and, 584 transition from diastolic dysfunction to, 197 Heart failure with preserved ejection fraction (HFpEF), 179 Heart rate, ejection fraction influenced by, 113 Heart transplantation See also Cardiac transplantation iatrogenic tricuspid valve flail in, 515–516, 516f Heart valve, transcatheter characteristics of, 814, 814t, 815t deployment of, 816–817, 816f postdeployment imaging for, 817 Hemangiomas, 620, 622f Hemochromatosis, 352 Hemodynamic stress testing, role of, in mitral stenosis, 468 Hemodynamics, pulmonary, in right ventricle, 340 Hemolysis, periprosthetic leaks and, 559 Hemosiderosis, diastolic dysfunction and, 196 Hepatic venous systolic filling fraction, 160 Hereditary familial systemic amyloidosis, 766 Heterograft valve, 544 Hiatal hernia, as pitfall of transesophageal echocardiography, 61 High-fidelity micromanometer catheter, 175 High-risk plaque, aortic, 661 High-risk right heart thrombi, 635–636 Holodiastolic flow reversal, 446–447, 446f in pulmonary artery, 535 Human immunodeficiency virus (HIV) atherosclerotic disease in, 787 cardiac tumors, 787 myocardial disease and cardiomyopathy, 786 pericardial disease, 786 pulmonary hypertension in, 786–787 as systemic diseases, 786, 786b valvular disease, 787 Hyperaldosteronism, 778, 779f Hypercortisolism, 778, 779f Hypereosinophilic syndrome (HES) cardiac involvement in, 773, 773b, 774b demographics and presenting symptoms, 773–774 diagnostics and therapeutics of, 774–775, 774f pathophysiology of, 774 classification of, 775b diastolic dysfunction and, 196 Hyperglycemia, diastolic dysfunction and, 195 Hypertension, 739 accelerates age-related arterial stiffness, 741 and/or left ventricular, 746 aortic dissection and, 673 Hypertension (Continued) arterial dynamics, 741 cardiac mechanics of, 739–740 chamber function, 739, 740t diastolic dysfunction and, 194, 195f dilated cardiomyopathy and, 322 echocardiographic indices of arterial dynamics in patients with, 741t of ventricular mechanics, 741t left ventricular size, 739, 740t mass of, 739, 740t pulmonary, 748 arterial See Arterial hypertension primary See Primary pulmonary hypertension (PPH) in sickle cell anemia, 784–785 and tricuspid regurgitation, 385 Hypertensive heart disease, 294–295, 748f Hyperthyroidism, 776–777, 778f Hypertrophic cardiomyopathy (HCM) anatomic variants of, 286, 286f, 287f apical See Apical hypertrophic cardiomyopathy clinical screening for, recommendations for, 312–313, 312t diastolic dysfunction and, 195 echocardiographic features of, 302 left ventricle in, 302 pathophysiologic classification of, 302–307 right ventricle in, 307 gene carriers of, 313 genetic testing in, 312 genetics of, 312 with left ventricular outflow tract obstruction See Left ventricular outflow tract obstruction (LVOTO) mid-ventricular obstruction in, 289 nonobstructive, 288–289, 306 obstructive See Obstructive hypertrophic cardiomyopathy pathophysiology of, 287–288 physiologic variants of, 288–289, 288f screening of relatives for, 312 versus secondary conditions that mimic HCM, 294, 295f, 298f athlete’s heart, 295, 296f hypertensive heart disease, 294–295 infiltrative disorders of myocardium, 295–297 isolated left ventricular noncompaction cardiomyopathy, 296f, 297, 298f storage diseases, 297–300, 298f syndromic hypertrophic cardiomyopathy, 300–301 therapy for, 307 alcohol septal ablation as, 309–311, 310f dual-chamber pacing as, 311 pharmacological, 307–308 surgical myectomy as, 308–309, 309f Hypertrophic septoparietal trabeculation, in tetralogy of Fallot, 726–727 Hypertrophy concentric, 739 LV, 739, 740f Hypotension and dyspnea, 807–808 myocardial infarction, acute complications of, 807–808 patient of, 808 Hypothyroidism, 776, 777f I Iatrogenic tricuspid valve flail, 515–516, 516f ICE See Intracardiac echocardiography (ICE) ICR See Inotropic contractile reserve (ICR) 867 Idiopathic dilated cardiomyopathy, 322 Image-based tracking, 846, 846f Image interpretation, basics of, 78–79 Imagify, 91–92, 92t iMAP IVUS, 78 Impaired active ventricular relaxation, 193 Impaired left ventricular function, left ventricular thrombus with, 624–625, 624f, 625f Impaired valve closure, 514–515 Incomplete leaflet closure, 502–504 Index streptococcal infection, 454 Indexed effective orifice area (IEOA), 550, 551f Inertial cavitation, of microbubble, 94 Infection as aortic repair complication, 698, 698f dilated cardiomyopathy from, 322 Infective endocarditis, 557, 575–592, 746 abscesses in, 576 cardioembolism and, 582, 582f diagnosis of, 577 Duke criteria for diagnosis of, 575b, 576b, 578t echocardiography in appropriate use of, 591t detection of complications of, 579 features of, 575 indications and diagnosis of, 578, 578f, 579f intraoperative, 586, 587f limitations and technical considerations for, 588, 589t, 590t surgical decision making and, 584–586, 585f transthoracic versus transesophageal, 577, 584 epidemiology of, 577 features of, 576 pathophysiology of, 577 therapy for, 579 types of, 577 vegetations in, 575–576 differential diagnosis of, 589b Inferior cava, valve of, 641, 641f, 642f Inferior vena cava plethora, 605, 605f low pressure, 605 Infiltrative cardiomyopathy clinical spectrum of, 349, 349f diagnosis of, 349–350 with dilated phenotype, 351–352 disorders causing, 349t hereditary and acquired, 348 with thick walls, 350–351 Inflammatory bowel diseases (IBDs), atrial fibrillation and, 634 Inflow cannula, 371, 372f Inotropic contractile reserve (ICR), 787f Inoue balloon catheter, 823 manipulation of, 826 Inspiratory annular enlargement, right ventricular widening associated with, 516 Instrument, echocardiographic, 1, 2f Interatrial communications (IACs) definition of, 65 device closure of, 65, 66f Interobserver variability, of LV systolic function assessment tool, 114 Intersocietal Commission for Accreditation of Echocardiography Laboratories (ICAEL), 850 Interventional echocardiography, 809–848 atrial interventions in, 809, 812f MitraClip procedure, 818 mitral balloon valvuloplasty, 823 patent foramen ovale, 840 septal defect closure, 831 in structural heart disease, 809t 868 Index Interventional echocardiography (Continued) three-dimensional echocardiography, fusion of, with fluoroscopy, 845 transcatheter aortic valve replacement, 814 transcatheter cardiac pseudoaneurysm closure, 837 transcatheter valve-in-valve implantation, 828 valvular interventions in, 809, 811f ventricular interventions, 809, 813f “Interventional imaging,” 539–540 Interventricular mechanical delay (IVMD), 129, 130f Intima, appearance of, in IVUS imaging, 78–79 Intracardiac echocardiography (ICE), 65–74 applications of, 65 in atrial septal defect closure, 832 cost-benefit ratio of, 72–73 and electrophysiologic ablation procedures, 65–66 and interatrial communications, 65 operator-dependent limitations of, 72 and patent ductus arteriosus, 68, 70f for patent foramen ovale closure, 844 rare and investigational applications of, 68–70 technical limitations of, 72 three-dimensional, limitations of, 72f, 73 and transcatheter aortic valve replacement, 67–68, 67f, 68f and ventricular septal defects, 68, 69f Intracardiac masses, 617, 618f echocardiography-guided biopsy of, 652 diagnostic evaluation of, 652–653 differential diagnosis of, 652 role of contrast echocardiography in assessment of, 647 differential diagnosis of, with contrast perfusion imaging, 648–649, 649f, 650f, 651f limitations of, 648–649 traditional echocardiographic diagnosis of, 647–648 use of contrast to detect and define of, 648, 648f Intracardiac pathology, delineation of, 99, 99f, 100f, 101f Intraluminal phased-array imaging (IPAI), 68 Intramural hematoma, 684–686, 685f, 686b, 686t as variant of aortic dissection, 674, 684–685 Intraobserver variability, of LV systolic function assessment tool, 114 Intraoperative echocardiography, 691 epiaortic scanning, 692–693, 693f in infective endocarditis, 586, 587f transesophageal, 691–692, 692f of tricuspid valve, 523 Intraoperative transesophageal echocardiography See Transesophageal echocardiography (TEE) Intrathoracic pressure, in inspiration, 608 Intravascular echocardiography, 75–84 See also Intravascular ultrasound Intravascular ultrasound, in penetrating atherosclerotic ulcer, 682, 684f Intravascular ultrasound (IVUS) applications of, 78–82, 79f, 80f data from, 75, 76f freestanding imaging console, 76f imaging technology, 75 instrumentation and technique in, 75 and lesion severity, 79–81, 81f limitations of, 82–83 modalities of, 76–78, 77f PCI assessment using, 81–82 performance of, 75–76, 77f Intravascular ultrasound (IVUS) (Continued) and plaque characteristics, 80f, 81 recommendations for use of, 82t types of, 78–79 vessel measurements, 81f Intraventricular dyssynchrony, 129 Intraventricular fluid dynamics, abnormalities of, 191 Intraventricular septum (IVS) hypertrophy, 302 IPAI See Intraluminal phased-array imaging (IPAI) Ischemia, dilated cardiomyopathy and, 335–336 Ischemic cascade, 241, 242f Ischemic heart disease 3D echocardiography for, 209 acute effects of, 209 echocardiographic detection of, 209–210, 210f echocardiography for, 209 false indications of, on echocardiography, 210–211 introduction to, 209 patterns of, and coronary artery, 210 strain echocardiography for, 209 Ischemic mitral regurgitation (IMR), 497–499, 500 asymmetric (regional) versus symmetric (global) remodeling patterns, 502t clinical and prognostic value of, 498 on clinical decision-making, 498–499 definition of, 500 echocardiographic features of, 501, 502b echocardiographic quantification of, 505, 506f indications of, 498 management of, 506 mechanisms of, 500–505, 500b, 503f, 507f pathophysiology of, 497–498, 499f prognosis of, 505 Isolated atrial amyloidosis, 344, 344t Isolated left ventricular noncompaction cardiomyopathy, 296f, 297, 298f Isovolumetric relaxation time (IVRT), 175 Isovolumic contraction time (IVCT), 117–118 Isovolumic relaxation time (IVRT), 117–118 IVCT See Isovolumic contraction time (IVCT) IVMD See Interventricular mechanical delay (IVMD) IVRT See Isovolumic relaxation time (IVRT) IVUS See Intravascular ultrasound (IVUS) J Jatene operation, 734 Jet area, 534 Jet density, 534 Jet length, 534 Jones criteria, in mitral stenosis, 454 K Kaposi sarcoma, 787 Kidney, and liver transplantation, 751 Kidney Disease Outcomes Quality Initiative (K/ DOQI), clinical practice guidelines for cardiovascular disease in dialysis patients, 748–750 for evaluation and management of chronic kidney disease, 750 L Laennec, Rene, 453 Lagrangian strain, 16 Lambl excrescences, 619–620 as pitfall of transesophageal echocardiography, 61, 61f Large left atrial myxomas, 466 Late systolic (PVs2), 181 Leakage volume, 556 Left anterior descending (LAD) coronary artery, 855 Left atrial appendage closure of device, ICE and, 69, 70f transesophageal echocardiography in, 57, 57f pectinate muscles in, 643, 643f prominent ridge of tissue between left upper pulmonary vein and, 643, 644f Left atrial myxoma, 619, 621f Left atrial remodeling definition of, 199 echocardiographic diagnosis, 199 Left atrial stasis, 627 Left atrial thrombus, 581–582, 627 additional diagnostic techniques of, 630 clinical implications of diagnosis of, 630–632, 632b, 632f pathogenesis formation of, 627 transesophageal echocardiographic diagnosis of, 627–629, 627f, 628f, 629f, 630f, 631f Left atrial volume, 199, 200f newer modalities of echocardiographic assessment of, 200 pitfalls in measurement of, 200, 202f Left atrium (LA), 199–208 contraction of, 627 dilation of, 199 enlargement of, 199 for outcome prediction and prognostication, 199 function of, 204–205, 204f assessment of, 203 challenges to measurement of, 207 volumetric indices of, 204t high-fidelity pressure recordings of, 186f size of assessment of, 199 diastolic dysfunction and, 199 echocardiographic methods of, 199–200 future directions of, 201–202 reverse remodeling of, 200–201 in stress echocardiography, 243, 253 Left upper pulmonary vein, prominent ridge of tissue between left atrial appendage, 643, 644f Left ventricle (LV) abnormalities of, 302 aneurysm in, 229 cavity of, transient ischemic dilation, 253 contraction of, 117 diagnostic criteria for, 241–243, 242f, 242t dilation, and remodeling, 224 dyssynchrony See Left ventricular dyssynchrony ejection fraction, and coronary artery disease, 220 evaluation of mechanics by tissue Doppler imaging and speckle tracking echocardiography, 16 function of, mitral regurgitation and, 496 functional anatomy of, 115–116, 116f high-fidelity pressure recordings of, 186f M-mode echocardiography of, 30, 31f mass estimation of, 27 myocardial segmentation of, 124, 125f myocardium, 126 performance determinants of, 118–120, 119f response to exercise, 120 response to pharmacologic stress, with dobutamine or vasodilators, 240t size and function, in cardiomyopathy, 228 Index Left ventricle (LV) (Continued) systolic function, 451 thrombus, and old myocardial infarction, 224 volume and dynamic geometry of, 116 wall abnormalities, and coronary artery disease, 209–210 wall motion, assessment of, 210 Left ventricular afterload, 118 Left ventricular apex, hemangiomas of, 620, 622f Left ventricular assist device (LVAD), 370–371 echocardiographic approach to, 370 evaluation after implantation of, 371, 371f, 372f malfunction considerations in, 371–372 postoperative troubleshooting of, 372 Left ventricular contractile reserve, prognostic value of, 274, 275f Left ventricular diastole, 173, 174f function clinical recommendations for echo labs for assessment of, 187 grading of, 188–189, 189f Left ventricular dysfunction, Takotsubo-like transient See Takotsubo cardiomyopathy Left ventricular dyssynchrony, assessment of, 128 echocardiographic approaches in, 129 electrical dispersion and mechanical dyssynchrony in, 128–129, 129f interventricular mechanical delay in, 129, 130f mapping latest mechanical activation for LV lead placement in, 133–136, 136f as marker of arrhythmias, 131–133 in myocardial disease with narrow QRS complex, 133 in patients with widened QRS complex for prognosis, 131 speckle tracking strain in, 130, 134f, 135f three-dimensional speckle tracking imaging in, 136–137, 137f tissue Doppler imaging in, 129, 131, 131f, 132f Left ventricular ejection fraction (LVEF), 625, 788 determination of, ultrasound contrast agents and, 98 dilated cardiomyopathy and, 333, 333f, 334f, 335f Left ventricular end-diastolic pressure (LVEDP), 177 Left ventricular endomyocardial fibrosis, 356f Left ventricular (LV) filling pressures difficult cases of, 187 estimation of, 185 with atrial fibrillation, 189 with depressed ejection fraction, 188, 188f with mitral regurgitation, 189 with normal ejection fraction, 188, 188f Left ventricular flow reserve assessment of, 418–419, 419f dobutamine stress echocardiography for, 418 Left ventricular free wall rupture, after myocardial infarction, 217 Left ventricular hypertension, 746 Left ventricular hypertrophy (LVH), 294, 740f unexplained, 295f Left ventricular noncompaction analysis of, echocardiographic, 366 diagnostic criteria for, 366–367, 367f features of, echocardiographic, 366, 366f isolated, 296f, 297, 298f tricks and tips in diagnosis of, 367–368, 368f Left ventricular opacification (LVO), 260t concepts behind, 265t contrast agents and, 269–270 imaging settings and presets for, 261t Left ventricular opacification (LVO) (Continued) myocardial contrast echocardiography for, 806, 806f protocols for, 265–266 Left ventricular outflow tract (LVOT) diameter, measurement of, and transcatheter heart valves, 817 measurement of, after transcatheter aortic valve implantation, 550–551 peak gradient of, measurement of, 292, 292f Left ventricular outflow tract obstruction (LVOTO), hypertrophic cardiomyopathy with, 289 assessment of Doppler, 304 echocardiographic, 292–293, 292f echocardiographic features of, 302–305, 303f functional features of, 290–292 pathophysiology of, 290 provocation of, 293 Left ventricular preload, 118 Left ventricular relaxation, 173 abnormal, 186b normal, 186b Left ventricular responses, in aortic regurgitation, 438, 439f, 440–441, 447–448 etiology, 438–439, 440f, 441f Left ventricular stiffness, 173–174 Left ventricular systolic dysfunction, regional in absence of coronary artery disease, 128b nonischemic causes of, 127–128 Left ventricular systolic function, 113–138 assessment tool for, in multimodality era, 113–115, 114t basic principles of, 115 cardiac cycle, 117–118, 117f, 118f functional anatomy, 115–116, 116f performance determinants, 118–120, 119f response to exercise, 120 volume and dynamic geometry, 116 dyssynchrony See Left ventricular dyssynchrony ejection fraction and, limitations of, 113, 114t evaluation of, indications for, 113, 114t global, 120 echocardiographic methods used to assess, 120–122 limitations and technical considerations, 122 parameters of, 122 regional, 124 correlation with coronary blood supply, 127, 127f correlation with extent of infarction, 127 LV myocardial segmentation, 124, 125f methods for assessment of, 124–127, 125t myocardial contractile function assessment by STE, 125–126, 125t, 126f visual assessment of, 125, 125t nonischemic causes of dysfunction, 127–128 Left ventricular thrombus, 581, 581f, 624 diagnostic tests and role of echocardiography in, 625–626 with impaired left ventricular function, 624–625, 624f, 625f predisposing conditions of, 624b with preserved left ventricular function, 625, 625f, 626f prognosis and treatment of, 626 Left ventricular wall motion, semiquantification of, using wall motion score index, 243 LEOPARD syndrome, 298f, 300–301 Lesion severity, IVUS and, 79–81, 81f Libman-Sacks endocarditis, 619–620 869 Lidocaine, for transesophageal echocardiography, 47 Limbus fossa ovalis, 162 Limited echocardiography, 85 versus focused cardiac ultrasound, 86t Lipomatous hypertrophy of atrial septum (LHAS), 642–643, 642t, 643f LMNA gene, 327 Loeffler endocarditis, 341–342 Longitudinal resolution, of IVUS, 75–76 Longitudinal strain (LS), 190 Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) trial, 200–201 Low cardiac output, 473 Low-flow, low-gradient aortic stenosis paradoxical, clinical and Doppler echocardiographic features of, 423b with preserved left ventricular ejection fraction, 422, 423f algorithm for diagnostic, 425f assessment of flow and stenosis severity, 424–425 clinical presentation and pathophysiology of, 422–424, 424f therapeutic management of, 425–426, 425f with reduced left ventricular ejection fraction, 417, 420f algorithm for, 418f assessing stenosis severity in, 419–421, 419f, 420f therapeutic management of, 421 Low peak pulmonic regurgitation velocity, 535 Lower risk right heart thrombi, 636 Lumen dilation, false, as aortic repair complication, 697–698 Lupus anticoagulant (LA), 761t LV See Left ventricle (LV) LV end-diastolic pressure (LVEDP), 445 LVEF See Left ventricular ejection fraction (LVEF) Lysosomal storage disorders, 299–300 M M-mode for constrictive pericarditis, 609, 609f for effusive constrictive pericarditis, 612, 612f for inferior vena cava plethora, 605, 605f and pericardial effusion, 593f of swinging of the heart, 606, 607f M-mode echocardiography, 30, 30f of aortic valve, 35–36 in hypertrophic obstructive cardiomyopathy, 36, 36f in normal motion, 35, 36f in premature opening, 36, 36f of cardiac tamponade, 37, 38f of constrictive pericarditis, 37–38, 38f for global LV systolic function assessment, 120, 123t as historical relic, 30 of left ventricle, 30, 31f limitations and technical considerations in, 122 limitations of, 30 of mitral valve, 30–35 in aortic insufficiency, 32f, 35 in color M-mode, 32f, 35 in left ventricular dysfunction, 32f, 35 mitral stenosis, 32, 32f normal motion, 30–31 prolapse, 32–35, 32f systolic anterior motion of anterior mitral leaflet, 32f, 35 of pericardial disease, 37, 38f of pulmonary valve, 36–37 870 Index M-mode echocardiography (Continued) in normal motion, 36, 37f severe pulmonary hypertension, 36–37, 37f of pulmonic regurgitation, 535 of pulmonic valve, 529 for regional LV systolic function assessment, 125t Magnetic resonance imaging (MRI) after aortic surgery, 698 in aortic assessment, 660 in aortic dissection, 674–675, 675f in blunt aortic trauma, 690 cardiac See Cardiac magnetic resonance (CMR) imaging in penetrating atherosclerotic ulcer, 682–683, 684t for pericarditis, 601, 601f of periprosthetic leaks, 562 Malignant tumors, 617 Malperfusion syndromes, as complication of aortic dissection, 674 Manufactured ultrasound contrast agents (UCAs), for left heart imaging, 637 MAPSE See Mitral annular plane systolic excursion (MAPSE) Masses, cardioembolism and, 582 Maximum flow velocity, location of, in bileaflet mechanical valves, 548f McConnell sign, 169, 169f Mean gradient, of tricuspid prosthetic valves, 566–567 Mean left atrial pressure (LAP), 185, 186f prediction of grades of, 187t Mean pressure gradient measurements, 460–462, 461f Mean pulmonary artery pressure (mPAP), 161 Mechanical circulatory support devices, for heart failure, 633 Mechanical dyssynchrony echocardiographic approaches to assess, 129 left ventricular, 128–129, 129f in myocardial disease with narrow QRS complex, 133 Mechanical index (MI), definition of, 94 Mechanical tricuspid valves, 567t Mechanical-valve endocarditis, 586–587 Mechanical valves, 539, 542–544 bioprostheses for, 528 obstruction in, 551–552, 555–556 Mercedes Benz sign, 399 Metabolic syndrome, 742 Metastatic lung cancer, 623, 623f Metastatic tumors, 623, 623f cardioembolism and, 582 Methemoglobinemia, 47 Methylene blue, for methemoglobinemia, 47 Microbeamforming, Microbubble contrast agents, 94–95 acoustic signal of, 95f clinical perspective in, 96–97 currently approved, 95f for myocardial perfusion, 212 physical properties of, 94, 95f Microbubble signal-to-noise ratio, 96, 97f Mid-ventricular obstruction, in hypertrophic cardiomyopathy, 289 echocardiographic features of, 305–306, 306f Midazolam, in transesophageal echocardiography, 47 Migraine, and patent foramen ovale, 843 Minimal myotonic dystrophy, 378 Mirroring, in spectral and color flow Doppler echocardiography, 63 MitraClip implantation, ICE and, 69 MitraClip procedure, 818 advancement of, into left ventricle, 821–822 assessment of result and MitraClip release, 822, 822f clip delivery system, advancement of, 821 effectiveness of, studies on, 818 implantation, additional, 822 indications and patient selection, 818–819, 818b leaflets, assessment of, 822, 822f mitral regurgitation severity, assessment of, 819t steerable guide catheter, introduction of, 821 steering and positioning of, 821 transesophageal echocardiography, 819, 819t, 820f three-dimensional, 819–821, 821f two dimensional echocardiography for, 819 Mitral annular calcification (MAC), 465, 465b, 644–645, 748t Mitral annular plane systolic excursion (MAPSE), 30 Mitral annular velocities, 182 Mitral annulus, 182, 302–303, 304f caseous calcification of, 644–645, 644b, 645f Mitral balloon valvuloplasty, 823 balloon mitral commissurotomy complications of, 826–828, 827f, 827t long term results of, 828 patient selection for, 823–824, 824t, 825t technique for, 824–826, 825f, 826f and three-dimensional transesophageal echocardiography, 824, 825f mitral stenosis, etiology of, 823, 824f Mitral deceleration time method, 180, 463 Mitral flow propagation, in amyloid, 768 Mitral flow velocity, Doppler measurement of, 179–180 Mitral inflow, 180f Doppler imaging of, 180 Mitral inflow method, for diastolic function, 175 Mitral leaflet tethering, 479 Mitral leaflets, 302, 304f Mitral periprosthetic leaks, 560–561, 561f percutaneous closure of, 563f Mitral prosthetic valve dysfunction, diagnosis of, 555–556 Mitral prosthetic valve regurgitation confirmation of, 557, 558f Doppler detection and quantitation of, 556 Mitral prosthetic valves, 555 standard transthoracic echocardiographic assessment of, 555 Mitral regurgitation (MR), 477–510, 748t, 756 after myocardial infarction, 217–218, 218f anatomy of, 478f, 485 assessment of, hemodynamics underlying, 485 asymptomatic severe, 492 indications for surgery, 492–493, 493b, 494t cardiomyopathy in, 228–229 chronic, due to geometric changes (remodeling) of left ventricle, 500–504, 501f degenerative, 478 differences in pathophysiologic features affecting, 444t dynamic, 496 estimation of left ventricular filling pressures with, 189 exercise echocardiography and, 495–496, 495t exercise stress echocardiography and, 240 exercise stress testing, role of, 495 functional, 500 Mitral regurgitation (MR) (Continued) ischemic, 497–499, 500 asymmetric (regional) versus symmetric (global) remodeling patterns, 502t clinical and prognostic value of, 498 on clinical decision-making, 498–499 definition of, 500 echocardiographic features of, 502b echocardiographic quantification of, 505 holosystolic regurgitation and, 504f indications of, 498 management of, 506 mechanisms of, 500–505, 500b pathophysiology of, 497–498, 499f prognosis of, 505 mechanism of, 290, 291f in acute rheumatic fever, 756f overview of, 477 P3 flail scallop, 478f primary, 496–497 clinical and prognostic value of, 496 clinical decision making, 496–497, 498f exercise-induced changes in, 497f indications of, 496 pulmonary venous flow patterns in, 491, 491f quantification of, 484, 485b severe, definition of, 485 supportive finding of, 490–491, 491f three-dimensional echocardiography, 488–490 anatomic regurgitant orifice area, 489, 490f convergence zone, reconstruction of, 490f derived quantitative measurements for, limitations of, 490, 491t mitral inflow and left ventricular outflow tract stroke volume, 489 proximal isovelocity surface area, 488–489, 489f vena contracta area, 488, 489f two-dimensional color Doppler, 485–488 jet area, 485–486, 486b, 486f vena contracta width, 486, 486f volumetric method, 487–488, 488f Mitral stenosis, 453, 454f, 748t acquired, nonrheumatic forms of, 466–467 consequences of, 471 etiology of, 454, 465b congenital, 467 mimic, nonrheumatic etiologies of, 465 quantification of, 460, 460f mean pressure gradient measurements, 460–462, 461f quantitative assessment of, 462t rheumatic, 454 chest radiography, 456 electrocardiography, 456 epidemiology of, 454–455 M-mode echocardiography of, 456f pathophysiology of, 455, 455f physical examination, 455–456 therapy of, 458 transesophageal echocardiography, 457, 457f, 459f, 466f, 467f transthoracic echocardiography, 456–457, 457f role of hemodynamic stress testing in, 468 schematic relating complications of, 472f secondary changes due to, 464 Mitral stenosis (MS), 823 etiology of, 823, 824f stress echocardiography for, indications of, 275, 275b Mitral supravalvular stenosing ring, 467 Mitral valve disease of, transesophageal echocardiography in, 55, 56f Index Mitral valve (Continued) interventions for, transesophageal echocardiography in, 57 Mitral valve, M-mode echocardiography of, 30–35 in aortic insufficiency, 32f, 35 in color M-mode, 32f, 35 in left ventricular dysfunction, 32f, 35 mitral stenosis, 32, 32f mitral valve prolapse, 32–35, 32f in normal motion, 30–31 systolic anterior motion of anterior mitral leaflet, 32f, 35 Mitral valve area change in, with exercise, 468–469 by continuity-equation method, 463 by Doppler techniques, 463–464 measurements, 462–464 mitral deceleration time method, 463 by planimetry, 463 pressure half-time, 463 by proximal isovelocity surface area method, 463–464 semiquantitative, by M-mode echocardiography, 464 Mitral valve disease, 478 Mitral valve dysfunction, 479–481 classification of, 479, 479f etiologies of, 477, 478 lesions associated with, 478–479 mechanisms of, 477 type I, 479f, 480f type II, 479, 479f, 480f type IIIa, 479f type IIIb, 479f, 481f Mitral valve prolapse, 478f, 481 color M-mode in patient with, 504f diagnosis of, 482–483, 483f etiology of, 482, 482f Mitral valve repair, 484, 570, 570f feasibility of, 493b likelihood of, 493–494 unsuccessful, predictors of, 494b Mitral valve surgery, 458 late development of tricuspid regurgitation following, 525–526 three-dimensional echocardiography for, 571–572, 571f, 572f Mitral valvuloplasty, 458, 474 M-mode echo-determined arterial stiffness, 741 M-mode echocardiography, 739 arterial stiffness, 741 mitral valve area by, semiquantitative, 464 Mobile calcific calcinosis, of heart, 748, 750f Moderator band, as pitfall of transesophageal echocardiography, 61, 61f “Modern stethoscope,” 87 Modified Jones Criteria, for diagnosis of acute rheumatic fever, 755b Monoleaflet valves, 543f, 544 Motorized pullback device, 75–76 mPAP See Mean pulmonary artery pressure (mPAP) MPI See Myocardial performance index (MPI) MR See Mitral regurgitation (MR) Mucopolysaccharidoses, 351 Multibeat acquisition, 6, 7f, Multiline acquisition, Multiplane imaging, simultaneous, 51, 65 Multiple thrombi, in left atrial body, 628f Muscular arteries, appearance of, in IVUS imaging, 78–79 Mustard operation, 734–735 Myectomy, surgical for hypertrophic cardiomyopathy, 293, 309f intraoperative echocardiography as guide to, 304–305, 306f Myocardial contrast echocardiography (MCE), 259 for adverse remodeling, detection of, 226 key image optimization for, 102f for left ventricular opacification, 806, 806f perfusion imaging in, 806–807, 806f, 807f Myocardial contrast stress echocardiography, offlabel, 105 diagnostic efficacy of, 105, 105t, 106t prognostic role of, 105 Myocardial disease, in HIV, 786 Myocardial hibernation, 255f Myocardial infarction acute, echocardiography in, 215 left ventricular outflow tract obstruction, 218, 219f left ventricular thrombosis, 216, 216f postinfarction ventricular septal rupture, 216–217, 216f right ventricular infarction, 218–219, 219f acute complications of, 807–808 versus cardiac death, in stress echocardiogram, 252 chronic remodeling, 223–225 early detection of, 225, 225f LV size and function in, 223, 224f manifestations of, 223–224 risk factors for, 224, 225f treatment and prevention of, 224–225 viability, 225–226 echocardiographic detection of, 209–210 inferior, coaptation and, 502f mitral regurgitation after, 217–218, 218f old, 222, 223f and ischemic MR, 226 papillary muscle rupture after, 217–218, 218f pseudoaneurysms after, 217, 217f Myocardial ischemia, and hypertrophic cardiomyopathy, 288, 288f Myocardial muscle deformation/strain, 190 Myocardial muscle mechanics, 190 Myocardial necrosis, and ischemic heart disease, 209 Myocardial performance index (MPI), 122, 183, 183f Myocardial reperfusion, for adverse remodeling, 225 Myocardial stunning, 254, 254f Myocardial tissue, 648 Myocardial viability, dilated cardiomyopathy and, 335–336 Myocarditis, 212 Myocardium, 190 infiltrative disorders of, 295–297 viable, 254 Myofibrils, left ventricular, 116, 116f Myotonic dystrophy, 378, 378f Myxomas, 582, 619, 621f Myxomatous degeneration, of mitral valve, 572f N Naloxone, in transesophageal echocardiography, 47 Needle pericardiocentesis, for pericardial effusions, 606 Neutral septum, of hypertrophic cardiomyopathy, 286f, 287f genotype status and, 287f Nodules of Arantius, 399 Non-Hodgkin lymphoma, 787 871 Noncompaction, left ventricular See Left ventricular noncompaction Nonlinear oscillation, of microbubble, 94–95 Nonobstructive hypertrophic cardiomyopathy, 288–289, 306 pathophysiologic classification of, 302 Nonresponders, 128–129 Nonsteroidal anti-inflammatory drugs (NSAIDs), for pericarditis, 602 Nonuniform rotational distortion (NURD), 75, 82–83 Noonan syndrome, 300–301 Normal Doppler values of mitral prosthetic valve function, 555 of prosthetic valve function, 551 Normal ejection fraction, estimation of left ventricular filling pressures with, 188, 188f Norwood procedure, 732 Nuclear stress testing, 279–281, 279f, 280t Nurse, role of, in using contrast agent, 92 Nyquist limit, 177 O Obesity cardiac assessment by echocardiography, 752–753, 752f diastolic dysfunction and, 195 Doppler echocardiography, 753–754, 753f pathophysiology of, 751–752, 752f as systemic diseases, 751 Obstruction, etiology of, in mitral prosthetic valves, 556–557, 557f Obstructive hypertrophic cardiomyopathy See also Left ventricular outflow tract obstructionMid-ventricular obstruction echocardiographic and Doppler assessment of, 292–293, 292f functional features of, 290–292 pathophysiologic classification of, 302 treatment of, 293, 307 Obstructive sleep apnea, and patent foramen ovale, 842 Off-line color tissue Doppler waveforms, 205 Optison, 92t Oscillatory component, of LV afterload, 118 “Ossification of the mitral valve,” 453 Outflow cannula, 371, 372f Outflow tract obstruction, left ventricular See Left ventricular outflow tract obstruction (LVOTO) Oxalosis, 351 P Pacemaker implantation, tricuspid regurgitation development/progression after, 515 PADP See Pulmonary artery diastolic pressure (PADP) Palliative shunts, for adult cyanotic complex congenital heart disease, 727–728, 727f Papillary fibroelastomas, 582, 619–620, 621f Papillary muscle dysfunction, 500 Papillary muscle rupture, 504–505, 505f after myocardial infarction, 217–218, 218f Para-annuloplasty ring leak, 559 “Para-ring” leak, 559 Parachute mitral valve, 467 Paradoxical embolism, 831 Parallel receive beamforming, 6, 6f Parasternal short-axis view, of pediatric echocardiogram, 708, 708f Paravalvular leaks, 539, 547 device closure of, imaging in, 69 872 Index Paravalvular regurgitation, 567–568 PASP See Pulmonary artery systolic pressure (PASP) Passive myocardial stiffness, increased, 193 Patches, Patent ductus arteriosus (PDA), 717, 717f ICE and, 68, 70f Patent foramen ovale, 840 anatomy and embryology of, 841, 841f clinical presentations, 841–842, 842t and cryptogenic stroke, 842–843 decompression sickness, 843 diagnosis of, 843–844, 843b, 843t interventional closure of, 844 medical management of, 844 and migraine, 843 pathophysiology, 841 and platypnea-orthodeoxia syndrome, 843 prevalence of, 840–841 Patent foramen ovale (PFO), 65 transesophageal echocardiography in, 57, 57f Pathologic regurgitation of aortic prosthetic valve regurgitation, 552–553, 553f of mitral prosthetic valve regurgitation, 556 PCI See Percutaneous coronary intervention (PCI) PDA See Patent ductus arteriosus (PDA) PE See Pulmonary embolism (PE) Pectinate muscles, in left atrial appendage, 643, 643f Pedoff probe, 400–401 Pencil probe, 400–401 Penetrating atherosclerotic ulcer (PAU), 680–681, 680f aortic dissection and, 674 etiology of, 680 imaging features of, 680–681, 681f, 682f, 683b imaging modalities for, 681–683 algorithm, 683, 684t angiography, 683 computed tomography, 681 intravascular ultrasound, 682, 684f magnetic resonance imaging, 682–683 transesophageal echocardiography, 681, 683f outcomes and prognosis of, 684 serial follow-up of, 683 treatment of, 683 PEP See Preejection period (PEP) Perceived exertion, Borg scale for, 246t Percutaneous aortic valves, in aortic regurgitation, 450 Percutaneous coronary intervention (PCI), IVUS and, 75–76, 81–82 Percutaneous interventional therapy, in aortic regurgitation, 450 Percutaneous mitral balloon valvuloplasty (PMBV), 458, 458t mitral valve intervention with, 470 Percutaneous mitral valvotomy, complications from, 474, 474f Perfusion defect, contrast, 103, 104f Pericardial cysts, 614 adjacent to left ventricle, 614f, 615f clinical presentation of, 614 differential diagnosis of, 614 giant, 615f imaging modalities, 614, 614f treatment of, 614 Pericardial diseases in HIV, 786 imaging modalities in evaluation of, 594t protocols for, 594t introduction to, 593 Pericardial diseases (Continued) M-mode echocardiography of, 37, 38f Pericardial effusion, 602–603 causes of, 603b echocardiographic quantification of, 603t echocardiography in, 603–604 fluid accumulation in, 603 mimics of, 603b epicardial fat as, 603b, 604f pleural effusions, 603b, 603f tuberculous, 611 Pericardial fat, 598, 598f as pitfall of transesophageal echocardiography, 61 Pericardial friction rub, 600 Pericardial tamponade, as complication of aortic dissection, 674 Pericardiocentesis echo-guided, 607 for pericardial effusions, 606 Pericarditis, 599, 747 acute, 214–215, 215f chest x-ray of, 600 clinical features of, 600 signs, 600 symptoms, 600 computed tomographic imaging of, 601 constrictive differentiating features of, 360t echocardiography for, 359, 360f, 360t, 361f etiology of, 358–359, 359t other investigations for, 359–362 pathophysiology of, 358–359 versus restrictive cardiomyopathy, 358 definition of, 599 diagnostic evaluation, 600 echocardiography, 600–601 electrocardiography, 600, 600f epidemiology of, 599 etiology of, 599–600 labs, 600 magnetic resonance imaging, 601, 601f calcified pericardium, 601, 602f with pericardial effusion, 601, 601f treatment of, 602 Pericardium, 595 absence of, 614–616 anomalies associated with, 615 cardiac computed tomography, 615–616 cardiac magnetic resonance for, 615–616 clinical presentation of, 615 diagnostic modalities for, 615 echocardiography, 615, 616f epidemiology, 614 pathogenesis, 615 treatment of, 615 effusions of, 598 extensions of, 599, 599f fat in, 598, 598f fluid in, 596–597 and intrapericardial pressure, 597, 598f intrapericardial versus extrapericardial heart structures, 597–598 normal anatomy of, 595, 596f, 602 phylogeny and embryology, 596 in pregnancy, 801 role of, 593 thickness of, 596, 597f visceral, 611 Peripartum cardiomyopathy, 322 Peripheral pulmonic stenosis, 722 Periprosthetic leaks (PPLs), 559 clinical presentation of, 559 diagnosis of, 559–561 imaging modalities of, 561–562 Periprosthetic leaks (PPLs) (Continued) prevalence of, 559 treatment of, 562–563 Perivalvular abscess, infective endocarditis and, 584 PFO See Patent foramen ovale (PFO) Pharmacology, in stress echocardiography, 238 Phased-array platform, of IVUS, 75, 76f Physicians role of, in using contrast agent, 92 sports medicine, 319 Physiologic/“normal” regurgitation of aortic prosthetic valve regurgitation, 552 of mitral prosthetic valve regurgitation, 556 “Physiological” tricuspid regurgitation, 517, 518f Plaques characteristics of, IVUS and, 80f, 81 detection of, contrast-enhanced carotid ultrasound in, 107, 108f Platypnea-orthodeoxia syndrome, and patent foramen ovale, 843 Pleural effusions as pericardial effusion mimic, 603b, 603f as pitfall of transesophageal echocardiography, 61 Point spread function, 7–8, 7f Post-cardiopulmonary bypass, transesophageal echocardiographic examination, 570f, 571, 571f Postexercise mean transmitral gradient, 469f Potts shunt, 727–728, 727f, 731 PPH See Primary pulmonary hypertension (PPH) Pre-cardiopulmonary bypass, transesophageal echocardiographic examination, 570 Precision test, of LV systolic function assessment tool, 114 Preejection period (PEP), 117–118 Pregnancy, 473–474 aortic dissection and, 674 cardiac chamber dimensions, 797, 798f cardiac output, 798 cocaine use in, 803 diastolic function, 798–800 echocardiographic changes during, 797t echocardiographic findings during, 797–801 left ventricular contractility and ejection fraction, 797–798 mitral inflow pulsed-wave Doppler during, 799f pericardium, 801 physiologic changes with, 797 pulmonary vein inflow pulsed wave Doppler during, 800f right ventricular systolic function, 798 systemic diseases, 797 tricuspid regurgitation, 800f valve function, 801 Pregnancy criteria, in antiphospholipid syndrome, 761t Premature tricuspid, 535 Preserved left ventricular ejection fraction, low-flow, low-gradient aortic stenosis with, 422, 423f algorithm for diagnostic, 425f assessment of flow and stenosis severity, 424–425 clinical presentation and pathophysiology of, 422–424, 424f therapeutic management of, 425–426, 425f Preserved left ventricular function, left ventricular thrombus with, 625, 625f, 626f Pressure half-time (PHT) method, 462–463 for aortic regurgitation measurement, 446–447 of tricuspid prosthetic valves, 567 Pressure recovery, 548 Index Primary amyloidosis, 344, 344t Primary benign tumors, 619–621, 621f, 622f Primary cardiac malignant neoplasms, 617 Primary cardiac tumors, 617 Primary leaflet abnormality, 441t Primary malignant tumors, 622–623, 622f Primary mitral regurgitation, 496–497 clinical and prognostic value of, 496 clinical decision making, 496–497, 498f exercise-induced changes in, 497f indications of, 496 Primary pulmonary hypertension (PPH), cor pulmonale and, 381 Primary tricuspid regurgitation, 511 Primary (intrinsic) valve disease, 511 Principal directions, 190–191, 191f PRKAG2 cardiomyopathy, 298f, 300, 300f PRKAG2 gene, 300 Prosthesis-patient mismatch (PPM), 548–549, 549t in aortic prosthetic valve dysfunction, 552 in mitral prosthetic valve dysfunction, 556 Prosthetic aortic valves, effective orifice areas for, 545t Prosthetic function, echocardiographic evaluation of, 528 Prosthetic mitral valves, for effective orifice areas for, 545t Prosthetic valves, 537, 828–829 aortic, 550 cardioembolism and, 582–583 classification of, 542 complications of, 539 different types of, 542 disease of, transesophageal echocardiography in, 56–57, 56f failure of, 564 general considerations for evaluation of, 537–538, 541f implantation and repair, 539–540 infective endocarditis and, 585, 591f mitral, 555 obstruction of, 551–552, 555–556, 556f overview and approach of, 537, 538f, 539f, 540f, 540t structures of, as pitfall of transesophageal echocardiography, 61, 61f surgical, 542–547 tricuspid, 564 Proximal isovelocity surface area (PISA), 35 for aortic regurgitation measurement, 447f, 448 mitral valve area by, 463–464 radius, of tricuspid regurgitation jet, 517, 520f tips for calculating, 487b two dimensional, method for mitral regurgitation measurement, 486–487, 487f Pseudoaneurysm cardiac, transcatheter closure of, 837 clinical course and treatment options, 838, 839f, 840f echocardiographic imaging in, 837–838 left ventricular pseudoaneurysm, 837–838 other imaging modalities for, 838 infarction-related, 838 left ventricular, 837–838 Pseudoaneurysms as aortic repair complication, 697, 697f ventricular, after myocardial infarction, 217, 217f Pseudoenhancement, of contrast-enhanced carotid ultrasound, 108 Pullback recordings, of IVUS, 75–76 Pulmonary angiography, in pulmonary embolism diagnosis, 167 Pulmonary arterial obstruction, pulmonary embolism associated with, 168 Pulmonary artery, holodiastolic flow reversal in, 535 Pulmonary artery catheter in a box, 159–161 pulmonary artery pressure, 160f, 161 pulmonary vascular resistance, 161 right atrial pressure, 159–160 right ventricular systolic pressure, 161 Pulmonary artery diastolic pressure (PADP), 161 Pulmonary artery pressure, 147–148 systolic, prognostic value of changes in transmittal pressure gradient and, 275, 275b, 276f Pulmonary artery systolic pressure (PASP), 161, 187 measurement postexercise, 470f resting, 470f Pulmonary autografts (Ross procedure), 546–547, 546f Pulmonary edema, 471 Pulmonary embolism (PE), 166, 213–214, 214f diagnosis of, 167, 167f prognosis of, 170, 170f transesophageal echocardiography in, 169–170 transthoracic echocardiography in, 167–169, 167b, 168b, 168f Pulmonary heart disease, echocardiography in, 381 See also Pulmonary hypertension Pulmonary hemodynamics, 340 Pulmonary hypertension (PH), 471–472, 496, 748, 771 aortic stenosis and, 409 arterial See Arterial hypertension in HIV, 786–787 primary See Primary pulmonary hypertension (PPH) in sickle cell disease, 784–785 and tricuspid regurgitation, 385 Pulmonary valve, M-mode echocardiography of, 36–37 in normal motion, 36, 37f severe pulmonary hypertension, 36–37, 37f Pulmonary vascular resistance (PVR), 161 Pulmonary vein (PV) extrapericardial location of, 598 flow velocity, accurate, 181, 181f Pulmonary venous flow, 181, 181f in constrictive pericarditis, 609 Doppler waveforms of, 205 PW Doppler of, 177, 178f Pulmonic balloon valvuloplasty, 764–765 Pulmonic insufficiency, 748t Pulmonic regurgitation (PR), 529–536 Doppler echocardiographic evaluation of, 529–530 epidemiology and etiology of, 529 evaluation overview of, 532 grading severity of, 531–532, 531t direct evaluation, 531 indirect evaluation, 532 impact of, on cardiac chambers, 535 markers of, 533f, 533t, 534f mechanism of, 532–533 semiquantification of, 532 semiquantitative assessment of, 533–535 surgical treatment of, 532 three-dimensional echocardiographic evaluation of, 529 trivial/mild degrees of, 532 two-dimensional echocardiographic evaluation of, 529 Pulmonic valve events of, 535 873 Pulmonic valve (Continued) imaging of, 532–533 involvement of, 764, 765f normal, 529 replacement of, 532 transesophageal echocardiography of, 529 transthoracic echocardiography of, 529 Pulmonic valve disease, transesophageal echocardiography of, 56 Pulmonic valve pulsed-wave, regurgitant fraction by, 535 Pulse-echo technique, Pulse repetition frequency (PRF), Pulse-wave (PW) Doppler cursor, 175 Pulsed wave (PW) Doppler, 12, 39–40, 40f in athletes, 321f in constrictive pericarditis, 609, 610f in evaluation of right ventricular function, 339 in left ventricular outflow obstruction assessment, 304 of pulmonic regurgitation, 530 Pulsed wave spectral Doppler pocket-sized ultrasound and, 85 of pulmonic regurgitation, 535 Pulsed wave tissue Doppler velocity, 767 Pulsus paradoxus, and cardiac tamponade, 606, 606f, 606t PV systolic fraction, 182 PVR See Pulmonary vascular resistance (PVR) Q Quadrature phase demodulation, 63 Quadricuspid aortic valve (QAV), 395, 395f, 438, 439f cardiac and noncardiac abnormalities associated with, 395b function of, 395t morphologic types of, 395t prevalence of, 395t R RA See Right atrium (RA) Radial strain (RS), 190 Radial strain dyssynchrony, 130 Ramus limbi dextri, 148 Rapid pressure recovery (RPR), 552 RASopathies, 300–301 See also LEOPARD syndrome, Noonan syndrome “Rastelli operation,” 734 Real-time imaging, 8–9 3D zoom, full-volume, live 3D, live 3D color, Real-time perfusion echocardiography (RTPE), 260t acquisition of images of, 263, 263f, 264f advantages and disadvantages of, 263 analysis of images in, 265, 265f, 266 concepts behind, 265t contrast use during stress echocardiography, 261 dobutamine, protocols for, 265–266, 266f imaging settings and presets for, 261t pitfalls and clinical tips for, 268 steps in performing, 267f Receiver operating characteristic (ROC) curves, 791f, 792f Reduced left ventricular ejection fraction low-flow, low-gradient aortic stenosis with, 417, 420f algorithm for, 418f 874 Index Reduced left ventricular ejection fraction (Continued) assessing stenosis severity in, 419–421, 419f, 420f therapeutic management of, 421 Reduction aortic aortoplasty, 695–696, 695f Reduction ascending aortoplasty, 695, 695f Regadenoson, and contrast administration, 103b Regional wall motion abnormality (RWMA), 99 Registration, in medical images, 845 automatic updating in, 846 Regurgitant fraction, by pulmonic valve pulsedwave, 535 Regurgitant jets, 517, 529–530 Regurgitant orifice, in tricuspid regurgitation, 517–519 Regurgitant volume and fraction, by comparing pulmonic to systemic flow, 535 Regurgitation of aortic prosthetic valves, 552–554 of mitral prosthetic valves, 556 tricuspid, 511–528 Relative apical sparring pattern, in cardiac amyloidosis, 345, 346f Renal disease, end-stage, 746 congestive heart failure and, 746 epidemiology of, 746–748 hypertension and/or left ventricular, 746 mobile calcific calcinosis of heart, 748 pericarditis, 747 pulmonary hypertension, 748 as systemic diseases, 746 valvular heart disease, 746 Renal failure, 747 Repeatability, of LV systolic function assessment tool, 114 Reperfusion therapy, for acute coronary syndrome, myocardial contrast echocardiography and, 807 Reservoir, for pulmonary venous return, 204 Resonant frequency, 94–95 Respiratory variation, of tricuspid regurgitation, 517, 521f Resting coronary blood flow, and ischemic heart disease, 210 Resting mitral valve mean gradient, 469f Restrictive cardiomyopathy, 607–608 classification of, 341, 341t, 342f, 343f and constrictive pericarditis, 358, 608t diastolic dysfunction in, 196 differentiating features of, 360t echocardiography for, 359, 360f, 360t, 361f etiology of, 359, 359t infiltrative cardiomyopathies and See Infiltrative cardiomyopathy Retest variation, of LV systolic function assessment tool, 114 Retrograde flow, premature cessation of, 534 Reverberation color flow, 63 in transesophageal echocardiography, 62 Reverse curvature, of hypertrophic cardiomyopathy, 286f, 287f genotype status and, 287f Reverse remodeling, of left atrium, 200–201 Reverse-to-forward velocity time integral, 530 Rhabdomyomas, 620 Rhabdomyosarcomas, 622 Rheumatic aortic stenosis, 396–397 Rheumatic fever epidemiology of, 754 pathogenesis of, 754 as systemic diseases, 754 Rheumatic heart disease, 454, 756 epidemiology of, 754 Rheumatic heart disease (Continued) multivalvular, 439f pathogenesis of, 754 systemic diseases, 754 Rheumatic mitral stenosis, 454 cardinal anatomic changes in, 465b chest radiography, 456 electrocardiography, 456 epidemiology of, 454–455 M-mode echocardiography of, 456f pathophysiology of, 455, 455f physical examination, 455–456 therapy of, 458 transesophageal echocardiography, 457, 457f, 459f, 465f, 466f, 467f transthoracic echocardiography, 456–457, 457f Rheumatic mitral valve disease, 478 Right atrial appendage (RAA) thrombi, atrial fibrillation and, 633–634 Right atrial pressure (RAP), 159–160, 530 secondary indices of, 160–161 hepatic vein flow velocity profile, 160 right atrial size, 161 right-sided E/e’ ratio, 161 Right atrium (RA), 151–152, 161 anatomy of, 161–162, 162f landmarks in, 162, 162f variants in, 162–163, 165b echocardiographic views of, 162, 163f enlargement of, clinical implications of, 165–166 performance of, 166 physiology of, 162 pressure of, 166 assessment by two-dimensional echocardiography, 166 size measurement of, 163–166 by three-dimensional echocardiography, 163–165, 165f by two-dimensional echocardiography, 163, 165f Right heart, echocardiographic evaluation of, 386, 387f Right heart failure, 472 Right heart pressure, evaluation of, 468 Right heart thrombi (RHT), 633 contemporary management strategies of, 639 conventional management strategies of, 638–639 echocardiography of, 634–635, 635f incidence of, 633 morphology and outcomes of, 635–636, 636f, 636t, 637f risk factors associated with, 633, 634t special at-risk clinical populations in, 633–634 specific echocardiographic imaging for, 636–637, 637f tissue characterization and contrast perfusion of, 637–638, 638f Right-to-left shunt, and RV infarction, 219, 219f Right ventricle (RV), 142, 151–152 anatomy of, 139–142, 140f coronary blood flow, 139, 140f echocardiographic assessment of, 139, 140f, 141f, 142f reference values for structure of, 139–141, 173f assessment of systolic and diastolic function of, 151 anatomy and physiology, 151–152 diastolic function See Right ventricular diastolic function quantitative evaluation by echocardiography of, 152–153, 152f RV size, 152–153 Right ventricle (RV) (Continued) size and function of, clinical impact of, 157 strain, 155–156, 156f, 157f systolic function See Right ventricular systolic function three-dimensional ejection fraction of, 155, 155f and cardiomyopathy, 228 in dilated cardiomyopathy, 337 dysfunction of See Right ventricular dysfunction echocardiography of, physiologic basis of, 142 coronary blood flow, 148–149, 149f diastolic function of, 149–150, 156–157 ejection and function, 145–146 hemodynamics, 146–148, 146t, 148f interventricular dependence of, 149, 149f, 150f newer imaging modalities, 150 rhythm disturbances originating from, 150 structure and anatomy, 142–145, 143t, 144f, 145f, 146f, 174f failure of, in tricuspid regurgitation, 516 function, 243, 524 hemodynamics of, 158 flow, 159, 159f pressure, 159 pulmonary artery catheter in a box, 159–161 resistance, 159 hypertrophy of, 307 pulmonary hemodynamics in, 340 remodeling of, 385 size and function of, evaluation of, 338, 338f, 339f studies for evaluation of, 338–340 Right ventricular cardiomyopathy, arrhythmogenic, echocardiography in, 362, 363b newer techniques for, 364, 364f, 365f versus other modalities, 364–365 right ventricular function in, 364 right ventricular structure in, 362–364, 363f Right ventricular diastolic function, 156–157 grading, 157 hepatic vein flow, 156 tissue Doppler echocardiography and strain, 156–157 lateral tricuspid annulus velocities, 156 tricuspid E/e’ ratio, 156–157 transtricuspid flow, 156 Right ventricular dysfunction, pathophysiology of, 337–338 Right ventricular endomyocardial fibrosis, 354f, 357f, 358f Right ventricular index of myocardial performance (RIMP), 153, 154f, 338–339 Right ventricular infarction, 148–149, 149f Right ventricular lead, 514–515 Right ventricular longitudinal strain (RVLS), 155 Right ventricular outflow view, of pediatric echocardiogram, 707, 707f Right ventricular pressure-volume loops, 146–147, 147f Right ventricular strain, 155–156, 156f, 157f Right ventricular stroke work index, 147 Right ventricular systolic function, 153–154 fractional area change, 153, 153f RV index of myocardial performance, 153–154, 154f tricuspid annular plane systolic excursion and velocity, 153 Right ventricular systolic pressure (RVSP), 161 Right ventricular widening, 516 RIMP See Right ventricular index of myocardial performance (RIMP) Index Ring-down artifact, IVUS and, 75, 82–83 RV See Right ventricle (RV) RVLS See Right ventricular longitudinal strain (RVLS) RVSP See Right ventricular systolic pressure (RVSP) S S/D ratio, 182 Sacks, Benjamin, 757 SAM See Systolic anterior motion (SAM) Sarcoidosis cardiac, 297 echocardiographic findings of, 769–771, 770f as systemic diseases, 769 Sarcomas, cardiac, 622 Sarcomere, 115, 116f SCN5A gene, 327 Screening, for hypertrophic cardiomyopathy, 312, 312t SDI See Strain delay index (SDI) Second harmonic imaging, 95–96 Secondary amyloidosis, 344, 344t Secondary cardiac tumors, 617 Secondary tricuspid regurgitation, 385, 517 Secondary (functional) valve dysfunction, 511 Segmental analysis, of adult CHD, 704–706 Seizures, cardioembolism and, 580 Self-expanding valves, 546f, 547–548 Semilunar valve, 718 Senile amyloidosis, 344, 344t Senile systemic amyloidosis, 766 Senning operation, 734–735 Sepsis, infective endocarditis and, 577 Septal bounce, 358–359 Septal defect closure, 831 atrial, 831–834, 832f, 833f, 834f ventricular, 834–836, 835f, 836f Septal leaflet, of tricuspid valve, 526 Septal perforator flow, 309 Severe mitral regurgitation, from BMC, 828 Sickle cell disease cardiac findings in, 785, 785f diastolic dysfunction, 784, 784f left ventricular structure and systolic function, 783–784, 783f limitations of, 785 pulmonary hypertension in, 784–785 screening considerations of, 785 as systemic diseases, 783 Sigmoid septum, of hypertrophic cardiomyopathy, 286f, 287f genotype status and, 287f Simpson biplane method, 200, 202f Single element platform, of IVUS, 75, 76f Single-photon emission computed tomography (SPECT), 237 stress echocardiography versus, 280t Situs ambiguus, 705, 705f Situs inversus, 705, 705f Situs solitus, 705, 705f 60/60 sign, 169, 169f Slope method, 177 Sonographer, role of, in using contrast agent, 92 Sonography, 1, 2f SonoVue, 91–92, 92t Sonazoid, 91, 92t Sparing pattern, apical, 350 Spatial resolution, of LV systolic function assessment tool, 113 Speckle tracking echocardiography (STE), 15–16, 15f in adverse remodeling, 225, 225f Speckle tracking echocardiography (STE) (Continued) evaluation of LV mechanics by, 16 for global LV systolic function assessment, 122, 123t for infiltrative cardiomyopathy, 350, 350f limitations and technical considerations for, 122 for myocardial function assessment, 125–126, 125t, 126f in RVLS assessment, 155–156, 156f Speckle tracking strain, 130, 134f, 135f, 272 Speckles, 15–16 Spectral broadening, 41 Spectral Doppler imaging echocardiography, artifacts concerning, 62–63 of left atrial function, 205, 205t of left ventricular pseudoaneurysms, 838 of tricuspid prosthetic valves, 568 Spectral Doppler velocity tracing, of tricuspid regurgitation, 519 Sphericity index, 223–224 Sports medicine physicians, 319 SR See Strain rate (SR) St Jude mechanical valves, 567 Stable cavitation, of microbubble, 94, 95f Stanford classification, of aortic dissection, 672–673, 673f Staphylococcus aureus, infective endocarditis from, 577 Starr-Edwards 1260, 542 STARTER (Speckle Tracking Assisted Resynchronization Therapy for Electrode Region), 135–136, 136f Static component, of LV afterload, 118 STE See Speckle tracking echocardiography (STE) Steinert disease See Myotonic dystrophy Stent implantation, IVUS and, 81–82, 82f Stented bioprostheses, 543f, 544–545, 544f Stented bioprosthetic valves, 542 Stentless bioprostheses, 545 Storage diseases, HCM and, 297–300 Strain myocardial, 122, 123f in speckle tracking echocardiography, 16 and strain rate imaging, of left atrial function, 205–207, 205t, 206f, 207f in tissue Doppler imaging, 15 Strain analysis, 228 Strain delay index (SDI), 130 Strain Doppler echocardiography, for detection of adverse remodeling, 226 Strain imaging for constrictive pericarditis, 610 of right ventricle, 150 two-dimensional, for right ventricular function, 339–340 Strain rate (SR), 14 measurement, 259 myocardial, 122, 123f Stress hypertensive response to, 240 left ventricular response to, 239–240 Stress cardiomyopathy, 128 Stress echocardiography, 237 advantage of, over other imaging techniques, 282, 282f aortic regurgitation and, 274 appropriate use criteria for, 277 stratification of diagnosis and prognosis, 278 for asymptomatic aortic stenosis, 426 clinical and prognostic value of, 427–430 impact on clinical decision-making, 430 875 Stress echocardiography (Continued) parameters of, 427 protocol for, 427, 428f comparison with other techniques, 279, 280t, 281f contrast, 102 interpretation of, 102–103, 104f left ventricular opacification, 103–104, 105t methodology in, 102, 102f myocardial, 105, 105t, 106t recommendations for, 103b contrast-enhanced, 260 for coronary artery disease, 220–221 prognostic value of, 221 current clinical practice of, 277–278, 278b diagnostic criteria and accuracy, 241, 243, 243t, 244t dobutamine, 246–247, 255–256 comparison with other modalities, 258 prognostic value of, 256–257, 256f, 257f protocol for, 256 rationale of, 255–256 steps in performing, 267f enoximone, 259 exercise, 245 aortic stenosis and, 240 bicycle ergometry, 246 diastolic dysfunction, 240–241 diastolic stress test, 247 effects of, 238 handgrip and, 247 mitral regurgitation and, 240 pharmacologic protocols for, 246–247 protocols of, 245–246, 245f exercise electrocardiography stress testing and, 279 hemodynamic effects of, 239 image acquisition, 248, 248f, 249f, 250f mechanism of ischemia in, 239 methodology of, 244 mitral stenosis and, 274 normal, warranty time of, 253 pacing on cardiovascular system, 238 pharmacological, 238 prognosis of, 251, 251b functional parameters and heart rate reserve, 252 risk stratification and wall motion abnormalities, 251–252, 252f value of, versus stress electrocardiography, 252 protocol, 274 specific protocols of, 263–265 three-dimensional, 268 2D stress echocardiography, comparison of sensitivity and specificity of, for detecting CAD, 273t advantages and disadvantages of, 269b analysis of, 272, 273f full volume acquisition, 268–269 left ventricle segment visualization, 269 modes of, 268–269 real-time imaging, 268 temporal resolution of, 269 volume data acquisition, 269 workflow and display, 270–271, 270f, 271f, 272f and timing of intervention, 470 valve disease and, 274 viability of, 254, 254t, 255t Stress testing diastolic, 247 exercise, role of, 495 nuclear, 279–281, 279f, 280t 876 Index Stressors comparisons of, 240 physiological responses to different kinds of, 239t Stroke, 580 TOAST criteria for, 580t Stroke volume (SV), 538 measurement of, 41 Stromal tumors, 637 Structural disease, CVD type, 747t Structural heart disease, 809 Structural valve degeneration (SVD), 551–552, 555–556 Stunning, myocardial, 254, 254f Subannular interventricular (RV/LV) ratio, 635, 635f Subaortic stenosis, 431 diagnosis of, 432–433, 433f, 434f, 435f epidemiology of, 431 etiology of, 431–432 morphology of, 431, 432f pathophysiology of, 431–432 treatment of, 433–435 Subcostal/subxiphoid long-axis, of pediatric echocardiogram, 707, 707f Subvalvar aortic stenosis, 721, 721f Sudden cardiac death (SCD) and ACAOs, athletes with, 230–231, 231f in athletes, 319f and coronary artery anomalies, 230 Suprasternal long-axis view, of pediatric echocardiogram, 707–708, 707f Suprasternal short-axis view, of pediatric echocardiogram, 707–708, 708f Supravalvar aortic stenosis, 721 Supravalvar pulmonic stenosis, 722 Surgical embolectomy, for right heart thrombi, 639 Surgical myectomy for hypertrophic cardiomyopathy, 293, 308–309, 309f intraoperative echocardiography as guide to, 304–305, 306f Sutureless bioprostheses, 546–547, 546f Sutureless stent-mounted bioprosthetic valves, 546, 546f Syndromic hypertrophic cardiomyopathy, 300–301 Systemic diseases, 739–804 amyloid, 765 antiphospholipid antibody syndrome, 760 carcinoid heart disease, 763 cardiac involvement in hypereosinophilic syndrome, 773 cardiotoxic effects of cancer therapy, 788 Chagas cardiomyopathy, 780 cocaine, 801 diabetes, 742 end-stage renal disease, 746 endocrine disease, 776 human immunodeficiency virus, 786, 786b hypertension, 739 lupus erythematosus, 757 obesity, 751 pregnancy and heart, 797 rheumatic fever, 754 rheumatic heart disease, 754 sarcoidosis, 769 sickle cell disease, 783 Systemic lupus erythematosus, 757 cardiac manifestations of, 758–760, 759t cardiovascular manifestations of, 758f demographics and presenting symptoms of, 761 diagnostic approach of, 758, 759f Systemic lupus erythematosus (Continued) etiology and pathophysiology of, 757–758 mechanisms of valvular dysfunction in, 758t pathophysiology of, 761–762 prevalence and outcome of, 758 Systemic sclerosis, diastolic dysfunction and, 196 Systolic anterior motion (SAM), 290 of anterior mitral leaflet, M-mode echocardiography of, 32f mechanisms of, 304, 305f Systolic chamber function, 740f Systolic hypertension, 450 Systolic pulmonary artery pressure, prognostic value of changes in transmittal pressure gradient and, 275, 275b, 276f T Takotsubo cardiomyopathy, 128, 212–213, 213f, 368, 368f, 369f, 370f presentation and findings of, 370t TAPSE See Tricuspid annular plane systolic excursion (TAPSE) TARGET trial, 133–135 Tau (τ), 173, 177, 182 TAVR See Transcatheter aortic valve replacement (TAVR) TDI See Tissue Doppler imaging (TDI) TEE See Transesophageal echocardiography (TEE) Tei index, 183, 183f Temporal resolution, 25 of LV systolic function assessment tool, 113–114 superior, of M-mode echocardiography, 30 Terminal ridge, 640–641, 641f Tetralogy of Fallot (TOF), 726–727, 726f Thallium scintigraphy, 258 Thebesian valve, 162 Thoracic aorta, 718 artifacts of, 645, 645f, 646f intraoperative transesophageal cardiography of, 691–692, 692f Three-dimensional color Doppler, for tricuspid regurgitation effective regurgitant orifice, 517–519, 522f Three-dimensional echocardiography (3DE), in aortic regurgitation, 448, 449f for cardiac tumors and masses, 617 fusion of, with fluoroscopy, 845 conclusion and future directions of, 848 cropping in, 847, 847f segmentation of, 847, 848f for global LV systolic function assessment, 120–122, 121f, 123t image acquisition and display, 8–9 data set cropping and rotation, 9f data set slicing, 10f three-dimensional data set display, 10f limitations and technical considerations in, 122 for mitral valve surgery, 571–572, 572f multiplane acquisition using the matrix array transducer, 5f physics, 6–8 impact of acquisition window on the spatial resolution of 3D data set, 8f parallel receive beamforming, 6–8 point spread function, 7–8, 7f stitching artifacts, 7f of prosthetic function, 528 in RA volume assessment, 163–165, 165f for regional LV systolic function assessment, 125t three-dimensional beamforming, 5f Three-dimensional echocardiography (3DE) (Continued) of tricuspid prosthetic valves, 569 two-dimensional beamforming, 4f versus two-dimensional echocardiography, 4–6 Three-dimensional imaging, of LV systolic function assessment tool, 114 Three-dimensional right ventricular ejection fraction (3D RVEF), 155 Three-dimensional strain, 190–191, 192f Three-dimensional stress echocardiography 2D stress echocardiography, comparison of sensitivity and specificity of, for detecting CAD, 273t advantages and disadvantages of, 269b analysis of, 272, 273f full volume acquisition, 268–269 left ventricle segment visualization, 269 modes of, 268–269 real-time imaging, 268 temporal resolution of, 269 volume data acquisition, 269 workflow and display, 270–271, 270f, 271f, 272f 3DE See Three-dimensional echocardiography (3DE) Thromboembolism, 539 Thrombolysis, for right heart thrombi, 639 Thrombosis, vascular, 761t Thrombus, 581–582, 581f, 582f echocardiographic features of, 169 left atrial, 627 left ventricular, 624 pedunculated, ultrasound contrast agents and, 99, 99f Tilting-disc valves, 537, 544 Tissue characterization, of right heart thrombi, 637–638, 638f Tissue displacement, 15 Tissue Doppler annular diastolic velocity, 182–183 Tissue Doppler imaging (TDI), 272 in athletes, 321f for constrictive pericarditis, 609–610, 610f for diastolic function, 175, 177, 177f evaluation of LV mechanics by, 16 for global LV systolic function assessment, 122, 123t of left atrial function, 205, 205t limitations and technical considerations in, 122 in LV dyssynchrony assessment, 129, 131, 131f, 132f principles of, 13–14 separating Doppler signals returning from tissue and blood, 14f for regional LV systolic function assessment, 125t in RVLS assessment, 155–156, 156f, 157f strain rate, strain and displacement, 14–15 calculations from velocity data and display, 15f two-dimensional displays of myocardial motion and deformation, 14f Tissue-Doppler strain imaging, 741 Tissue harmonic imaging, 17 advantages, 17 applications and their purposes, 18t disadvantages, 17 versus fundamental imaging, 18t generation for transthoracic imaging, 17f harmonic signal created by given tissue and its fundamental amplitude, 17f key application principles, 17–18 valve thickness that occurs when switching from fundamental imaging to THI, 18f Tissue valves, 544–545 Titin (TTN), 174 Index To-and-fro flow, 534–535 TOF See Tetralogy of Fallot (TOF) Torsion, 190 novel measures of cardiac function in diabetes, 744 Total cavo-pulmonary anastomosis, 735–736 TPM1 gene, 327 Transannular patch, 733 Transaortic velocities, 400–401, 402f Transcatheter aortic valve implantation (TAVI), 542 measurement of left ventricular outflow tract parameters after, 550–551 Transcatheter aortic valve replacement (TAVR), 814 ICE and, 67–68, 67f, 68f patient selection in, 814 postimplantation follow-up, 817–818, 817f preprocedural imaging for, 814–816, 815f procedural imaging, 816–817, 816f transcatheter heart valve characteristics of, 814, 814t, 815t deployment of, 816–817, 816f postdeployment imaging for, 817 Transcatheter bioprosthetic valves, 547–548 Transcatheter cardiac pseudoaneurysm closure, 837 clinical course and treatment options, 838, 839f, 840f echocardiographic imaging in, 837–838 left ventricular pseudoaneurysm, 837–838 other imaging modalities for, 838 Transcatheter heart valve characteristics of, 814, 814t, 815t deployment of, 816–817, 816f postdeployment imaging for, 817 Transcatheter valve-in-valve implantation, 569, 828 complications of, 829, 830f imaging for, 829 procedure, 829 valve in valve, 829 Transcatheter valves, flow pattern of, 547–548, 547f Transducers in echocardiography, 1, 2f two- and three-dimensional, 4f Transesophageal echocardiography (TEE), 47–64, 65, 457, 457f, 459f, 466f, 467f, 691, 759–760 3D, for anomalous CAs, delineation of, 234 in adult CHD, 708 after aortic surgery, 698 in aortic assessment, 659 in aortic dissection, 214 diagnosis, 675, 677f, 678f, 679f aortic plaque and, 661, 661b, 662f in aortic regurgitation, 448 applications of, 55, 58b artifacts of, 62 acoustic shadowing as, 62, 62f low imaging quality, 62 reverberation, 62 side lobe and beam width artifacts, 62 for atrial septal defect closure, 832, 833f in blunt aortic trauma, 690 of cardiac structures, 617 for cardioembolism, 581 contraindications to, 48t in cor triatriatum, 466 for coronary artery anomalies, 232, 234f in critically ill patients, 58 image-based tracking in, 846, 846f in infective endocarditis detection of complications of, 579 Transesophageal echocardiography (TEE) (Continued) indications and diagnosis of, 578, 578f, 579f intraoperative, 586, 587f sensitivity and specificity of, 588, 589f, 589t, 590t versus transthoracic echocardiography, 577, 584 intraoperative, 691–692, 692f for left atrial thrombus, 627 clinical implications of diagnosis of, 630–632, 632b, 632f for left ventricular thrombus, 224, 626 limitations of, in aortic prostheses, 553–554, 554f for MitraClip procedure, 819–821, 820f of mitral prostheses, 556–557 for patent foramen ovale, closure of, 844 in penetrating atherosclerotic ulcer, 681, 683f, 684t perioperative, 234 pitfalls of, 59–61 probe insertion in, 48 probe manipulation, 48–49, 49f anteflexion and retroflexion, 48, 49f general points in, 49 insertion and withdrawal, 48, 49f lateral steering, 48, 49f omniplane angulation in, 48, 49f rotation, 48, 49f in prosthetic tricuspid valves, 568 in prosthetic valves, 537, 540b protocol for, 47 in pulmonary embolism, 169–170 of pulmonic regurgitation, 529 risks and complications in, 49, 49t sedation in, 47 in sinus of Valsalva aneurysm diagnosis, 669, 669f, 670f in surgical myectomy, 308–309, 308f three-dimensional, 846, 846f for atrial septal defect, characterization of, 832, 833f in balloon mitral commissurotomy, 824, 825f for MitraClip procedure, 821f, 822f tomographic view, 50, 65 deep transgastric five-chamber view, 53 descending aorta SAX and LAX view, 54 midesophageal ascending aorta short-axis view, 52 midesophageal AV LAX view, 51 midesophageal AV SAX view, 52 midesophageal bicaval view, 52 midesophageal five-chamber view, 50 midesophageal four-chamber view, 50–51 midesophageal left atrial appendage view, 53 midesophageal long-axis view, 51 midesophageal mitral commissural view, 51 midesophageal modified bicaval TV view, 52 midesophageal right and left pulmonary veins view, 53 midesophageal right pulmonary vein view, 52 midesophageal right ventricle inflowoutflow view, 52 midesophageal two-chamber view, 51 transgastric apical SAX view, 53 transgastric basal SAX view, 53 transgastric long-axis view, 54 transgastric midpapillary SAX view, 53 transgastric right-ventricle inflow view, 54 transgastric RV basal view, 53 transgastric RV inflow-outflow view, 53 transgastric two-chamber view, 53 877 Transesophageal echocardiography (TEE) (Continued) upper esophageal aortic arch long-axis view, 54 upper esophageal aortic arch short-axis view, 54 topical anesthesia in, 47 for transcatheter aortic valve replacement, 816 for ventricular septal defect closure, 836 Transient ischemic attack See Stroke Transposition of great arteries (TGA) complete, 727 repair of, case example of, 734, 734f, 735f, 736f physiologically “corrected,” 728–729, 729f, 730f Transthoracic echocardiography (TTE), 19–46, 759–760, 797 for ACAOS, 230 in alcohol septal ablation, 310–311, 310f in aortic aneurysm diagnosis, 663–664 in aortic assessment, 659 apical window, 21–22 two-chamber view, 22, 22f three-chamber (long-axis) view, 22, 23f four-chamber view, 22, 22f five-chamber view, 22, 22f and appropriate use criteria appropriate indications from, 850b inappropriate indications from, 850b in athletes, 319–320, 320f, 320t for cardiac mass, 617 for cardioembolism, 581 for coronary artery anomalies, 232 imaging of valve with, 537 imaging protocol for, 232–234 in infective endocarditis, 577 detection of complications of, 579 indications and diagnosis of, 578 sensitivity and specificity of, 588, 589f, 589t, 590t versus transesophageal echocardiography, 577, 584 for left atrial thrombus, 630, 631f for left ventricular thrombus, 224, 624 nomenclature and standard views for, 19, 20f parasternal long-axis view, for transcatheter aortic valve replacement, 815 parasternal window, 19–21 left ventricle, long axis view of, 19, 20f long-axis view, 26–27, 27f right, 21, 21f right ventricular inflow and outflow, 26–27, 27f right ventricular inflow and outflow, long axis view of, 19, 20f short axis, 19–21, 20f, 21f short-axis view, 26–27, 28f and patent foramen ovale, 844 of prosthetic valves, 550, 555 in pulmonary embolism, 167–169, 167b, 168b, 168f, 169f of pulmonic regurgitation, 529 rheumatic mitral stenosis, 456–457, 457f subcostal window, 23, 23f, 29, 29f suprasternal notch window, 23–24, 24f technical quality of, 24 2D images, 24–25, 24f color Doppler images, 25, 26f spectral Doppler traces, 25, 25f tomographic views of, 26 off-axis, 29 transthoracic apical window, 27–29, 28f transthoracic suprasternal window, 29, 29f two-dimensional, for right heart thrombi, 634 878 Index Transvalvular regurgitation, 567–568 Transverse sinus extensions of, 599 fluid in, 643–644, 644f Trastuzumab (Herceptin), 789 Traumatic organic tricuspid regurgitation, 514, 514f risk factors of, 515 Treadmill exercise, and contrast administration, 103b for exercise echocardiography, 239, 245–246 exercise protocols used in, 245f steps in performing, 267f Tricuspid annular dilation, 511, 524–525, 524f, 525f Tricuspid annular plane systolic excursion (TAPSE), 30, 146, 339 measurement of, 145f Tricuspid annular plane systolic velocity, 153 Tricuspid annulus dilation and dysfunction of, 385 fat infiltration of, 643 Tricuspid insufficiency, 748t Tricuspid prosthetic valves, 564 echocardiographic assessment of, 564–567 regurgitation of, 567–568, 567t Tricuspid regurgitant volume, 517, 521f Tricuspid regurgitation (TR), 511–528, 800f comparison of ACC/AHA guidelines and ESC guidelines in management of, 524t echocardiographic assessment of, 519–522, 522t echocardiographic evaluation of, 384 epidemiology of, 511, 512f etiology of, 511–516, 512b, 513f, 514f, 515f, 516f late development of, following mitral valve surgery, 525–526 mechanisms of, 511–516, 513f, 514f, 515f, 516f natural history of, 516 pulmonary hypertension and, 382, 383f, 385 quantification of, 517 severity of, 523 Tricuspid regurgitation jet, vena contracta of, 517, 519f, 520f Tricuspid valve (TV), 162, 511, 512f, 764f echocardiographic findings of, involvement, 764, 764f indications for surgery of, 523 procedures of, 526 replacement of, 528, 528f, 764 tethering of, 385 Tricuspid valve annuloplasty, 385 Tricuspid valve annulus, 524, 524f Tricuspid valve disease, transesophageal echocardiography of, 56 Tricuspid valve leaflets, mechanisms of electrocatheter wire interference with, 514–515, 515f Tricuspid valve prosthesis dysfunction, 564 TTE See Transthoracic echocardiography (TTE) TTN gene, 326–327 Tuberculous pericardial effusions, 611 Tumors, metastatic, cardioembolism and, 582 Turbulent versus laminar regurgitant jet, 534 TVI ratio, for tricuspid valve prostheses, 567 Two-dimensional color Doppler jet area, 485–486, 486b, 486f Two-dimensional echocardiography (2DE) for diastolic heart failure, 175 for global LV systolic function assessment, 120, 121f, 123t limitations and technical considerations in, 122 in RA dimensions and volume measurement, 163, 165f in RA pressure assessment, 166 Two-dimensional echocardiography (2DE) (Continued) for regional LV systolic function assessment, 125t of tricuspid prosthetic valves, 564, 568 for tricuspid regurgitation, 517 Two-dimensional imaging of mitral prosthetic valves, 555 of prosthetic valve function, 550 Two-dimensional strain imaging, for right ventricular function, 339–340 Two-dimensional stress echocardiography 3D stress echocardiography, comparison of sensitivity and specificity of, for detecting CAD, 273t potential limitations of, 269b Two-dimensional vena contracta width, 486, 486f Two-handed approach, in transesophageal echocardiography probe insertion, 48 2DE See Two-dimensional echocardiography (2DE) Type B thrombi, 636 U Ultrasound, focused, 88 applications of, 88, 88b goals of, 88b limitations of, 88–89, 88b hand-carried, 85 background of, 85 color Doppler and, 85 instrumentation of, 85, 86f spectral Doppler and, 85 technique in, 85–87, 86f, 87b intravascular See Intravascular ultrasound for patent foramen ovale, 843, 843t and pericardium, 593–595 Ultrasound contrast agents, 91, 92t applications for stress echocardiography, 260, 260t, 261t clinical applications of, 98–99 cardiac function assessment in, 98–99 delineation of intracardiac pathology in, 99, 99f, 100f, 101f composition of, 92, 92t microbubble, 94–95 acoustic signal of, 95f currently approved, 95f physical properties of, 94, 95f nurse in using, role of, 92, 263 physician in using, role of, 92, 262–263 physiologic basis for examining myocardial perfusion with, 261–262, 262f safety of, 92–93, 93t sonographer in using, role of, 92, 263 technical considerations for, 92, 262 Ultrasound stethoscope, cardiac physical examination targets for, 87b Undiseased coronary artery, IVUS imaging of, 79f Univentricular heart, 727 V V/Q scan See Ventilation-perfusion lung scan (V/Q scan) “V” wave cutoff sign, 519 Valsalva aneurysm, sinus of, 666, 667f clinical significance of, 666–669, 667f, 667t, 668f diagnosis of, 669–670, 669f, 670f etiology of, 667t treatment of, 671 Valsalva maneuver, for diastolic function, 177, 180 Valvar aortic stenosis, 719, 719f Valvar pulmonary stenosis, 721 Valve degeneration, 539 Valve disease, stress echocardiography, 274 Valve replacement surgery, 542, 559 Valvular disease, 537, 559 Valvular dysfunction, 539 in systemic lupus erythematosus and consequences, 758t Valvular heart disease, 746 from SLE, 759 Valvular insufficiency, 531 Valvular lesions, sources of cardioembolic embolization, 657 Valvular surgery, transesophageal echocardiography in, 57 Vascular resistance, 159 Vascular thrombosis, 761t Vasodilator stress myocardial perfusion imaging, 266–268, 266b acquisition of, 266, 267f analysis of, 266–268 clinical parameters, 266b RTPE pharmacologic stress, 266t Vegetations, in infective endocarditis, 575–576 differential diagnosis of, 589b Velocity-time integral (VTI), 40, 41f Vena contracta, 534 of tricuspid regurgitation jet, 517, 519f, 520f width for aortic regurgitation, 447f, 449f two-dimensional, 486, 486f Ventilation-perfusion lung scan (V/Q scan), in pulmonary embolism diagnosis, 167 Ventricular arterial coupling, 174 Ventricular free wall rupture, 807–808 Ventricular looping, 726 Ventricular septal defect (VSD), 710–711, 710t, 712f, 713f, 714f, 715f, 716f after surgical myectomy, 309f closure, 834–836 indications for, 834 percutaneous, 835, 835f, 836f surgical, 834 ICE and, 68, 69f sinus of Valsalva aneurysm and, 666–668 Ventriculoarterial concordance, 706 Ventriculoarterial discordance, 706 Ventriculoplasty, surgical, for adverse remodeling, 225 Verapamil, for obstructive hypertrophic cardiomyopathy, 293 VH IVUS Imaging System, 77f, 78 Viable myocardium, 254 Visceral situs, 705, 705f Visual artifacts, IVUS and, 82–83 Volume imaging, Volume rate, Volume rendering modality, Volumetric methods, of left atrial function, 205 Vortices, 191 VSD See Ventricular septal defect (VSD) VTI See Velocity-time integral (VTI) Vulnerable plaque, 108 W Wall motion abnormalities of duration of regional, 252–253 evaluation for, 805, 805b heart rate and, 252 at low heart rates, 243 risk stratification and, 251–252 right ventricular, role of, 253 Wall motion score index, semiquantification of left ventricular wall motion using, 243 Wall-thump filter, 12 Index Warfarin, for patent foramen ovale, 844 “Washing jets,” 556 Waterston shunt, 727–728, 731 Wide-open regurgitation, 517, 518f Wilkins Echocardiographic score, for valve morphology, 824, 825t X Z Xenograft prosthetic valves, 567 Zero baseline reference, 205–207 Y Y descent, in constrictive pericarditis, 608 879 This page intentionally left blank ... Cardiol 60 :23 25 23 29, 20 12 12 Weidemann F, Herrmann S, St€ork S, et al.: Impact of myocardial fibrosis in patients with symptomatic severe aortic stenosis, Circulation 120 :577–584, 20 09 13 Azevedo... J Am Coll Cardiol 63 (22 ) :24 38 24 88, 20 14 Vahanian A, Alfieri O, Andreotti F, et al.: Guidelines on the management of valvular heart disease, Eur Heart J 33 :24 51 24 96, 20 12 Lancellotti P, Lebois... 361: 124 1– 124 6, 20 03 Vahanian A, Baumgartner H, Bax JJ, et al.: Guidelines on the management of valvular heart disease, Eur Heart J 28 :23 0 26 8, 20 07 Bonow RO, Carabello BA, Chatterjee K, et al.: 20 08